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HerrPostmann 6:17am on Thursday, October 21st, 2010 
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sebhen 9:59am on Wednesday, May 26th, 2010 
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landlord 6:53am on Friday, April 30th, 2010 
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Valentin.Nes. 8:30pm on Friday, March 26th, 2010 
Bought this at $599 minus $50 rebate. Well worth the money, just wait for a sale price. The bottom door thing hopefully was a one time thing. Makes me wonder what else may have gone by unnoticed.
jhartman 4:51am on Tuesday, March 23rd, 2010 
NEVER BUY HP. They will con you out of your hard earned money and give you some low-end POS hardware that they call a laptop.
OONewbie 11:59am on Sunday, March 14th, 2010 
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jbugden 4:16am on Saturday, March 13th, 2010 
HP PAVILION 2112SA Pros This laptop is excellent for entertainment Cool design Superb processor 2.

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Am J Physiol Renal Physiol 296: F590F597, 2009. First published January 7, 2009; doi:10.1152/ajprenal.90703.2008.
Rho-kinase inhibition reduces pressure-mediated autoregulatory adjustments in afferent arteriolar diameter
Edward W. Inscho, Anthony K. Cook, R. Clinton Webb, and Li-Ming Jin
Department of Physiology, Medical College of Georgia, Augusta, Georgia
Submitted 21 November 2008; accepted in nal form 5 January 2009
Inscho EW, Cook AK, Webb RC, Jin L-M. Rho-kinase inhibition reduces pressure-mediated autoregulatory adjustments in afferent arteriolar diameter. Am J Physiol Renal Physiol 296: F590F597, 2009. First published January 7, 2009; doi:10.1152/ajprenal.90703.2008.Preglomerular resistance is regulated by calcium inux- and mobilizationdependent mechanisms; however, the role of Rho-kinase in calcium sensitization in the intact kidney has not been carefully examined. Experiments were performed to test the hypothesis that Rho-kinase inhibition blunts pressure-mediated afferent arteriolar autoregulatory behavior and vasoconstrictor responses evoked by angiotensin II and P2X1 receptor activation. Rat kidneys were studied in vitro using the blood-perfused juxtamedullary nephron technique. Autoregulatory behavior was assessed before and during Rho-kinase inhibition with Y-27632 (1.0 M; n 5). Control diameter averaged 14.3 0.8 m and increased to 18.1 0.9 m (P 0.05) during Y-27632 treatment. In the continued presence of Y-27632, reducing perfusion pressure to 65 mmHg slightly increased diameter to 18.7 1.0 m. Subsequent pressure increases to 130 and 160 mmHg yielded afferent arteriolar diameters of 17.5 0.8 and 16.6 0.6 m (P 0.05). This 11% decline in diameter is signicantly smaller than the 40% decrease obtained in untreated kidneys. The inhibitory effects of Y-27632 on autoregulatory behavior were concentration dependent. Angiotensin II responses were blunted by Y-27632. Angiotensin II (1.0 nM) reduced afferent diameter by 17 1% in untreated arterioles and by 6 2% during exposure to Y-27632. The P2X1 receptor agonist, , -methylene ATP, reduced afferent arteriolar diameter by 8 1% but this response was eliminated during exposure to Y-27632. Western blot analysis conrms expression of the Rho-kinase signaling pathway. Thus, Rho-kinase may be important in pressure-mediated autoregulatory adjustments in preglomerular resistance and responsiveness to angiotensin II and autoregulatory P2X1 receptor agonists. P2 receptors; P2X1 receptors; ATP; Y-27632; autoregulation
by agonist-induced and pressure-mediated adjustments in preglomerular resistance (51). Accurate regulation of preglomerular resistance is central to the maintenance of glomerular capillary pressure. Afferent arterioles are the main vascular elements responsible for pressure-mediated autoregulatory adjustments in preglomerular resistance for the regulation of renal blood ow and glomerular ltration rate (9, 51, 53). Autoregulatory changes in renal vascular resistance are calcium dependent and involve the combined inuences of the myogenic and tubuloglomerular feedback mechanisms (4, 12, 21, 28, 49, 52, 53, 58, 61). Inux of calcium from the extracellular medium is an essential signaling pathway leading to autoregulatory vasoconstriction (12, 52, 53, 58). Blockade of L-type calcium channels, or removal of calcium from the extracellular medium, inhibits
autoregulatory vasoconstriction (10, 21, 23, 49, 58). These data demonstrate the essential role elevation of intracellular calcium concentration plays in autoregulatory vasoconstriction (10, 21, 23, 49, 58). Interestingly, the role of changes in calcium sensitivity to the renal autoregulatory response, or to the afferent arteriolar response to vasoconstrictor agents, has not been extensively investigated (50). Evidence indicates that renal microvessels express P2X1 and P2Y2 receptors and that P2X1 receptors are important for affecting pressure-mediated autoregulatory vasoconstriction of afferent arterioles (26, 27, 30). P2X1 receptors stimulate afferent arteriolar vasoconstriction by stimulating calcium inux largely through voltage-dependent L-type calcium channels (25, 3234, 67). In contrast, P2Y2 receptors stimulate vasoconstriction mainly by mobilizing calcium from intracellular stores (25, 32). Inactivation of P2X1 receptors blocks pressuremediated autoregulatory vasoconstriction leading to the postulate that increases in transmural pressure lead to ATP-mediated activation of P2X1 receptors to produce the autoregulatory vasoconstriction response (26, 30). Elevation of intracellular calcium concentration is an important component of afferent arteriolar autoregulatory responses and in the response of these arterioles to vasoconstrictor agonists. Considerable evidence supports an essential role of intracellular calcium in the afferent arteriolar response to pressure, angiotensin II, norepinephrine, endothelin, and to P2 receptor agonists (8, 19, 20, 28, 31, 40 43, 50, 64). While increasing the intracellular calcium concentration facilitates contraction of vascular smooth muscle, studies indicate that enhancing the sensitivity of the contractile apparatus to calcium is also important (6, 38, 39, 48, 50, 60, 66). Many investigators examined the calcium signaling pathways involved in the renal vascular response to vasoconstrictor stimuli but little has been done to determine the contribution of altered calcium sensitivity in these responses (48). The mechanisms underlying modulation of calcium sensitivity are poorly understood. Previous work focused on protein kinase C, but recently attention has shifted to the possible contribution of Rho and the Rho-associated family of proteins as a way to modulate calcium sensitivity (3, 6, 16, 35, 62, 65). Activation of a small GTP-binding protein, RhoA, stimulates Rho-kinase activation, which inhibits myosin light chain phosphatase, thus enhancing the interaction between actin and the myosin light chains (2, 45). Cavarape and colleagues (14) reported that Rho-kinase inhibition with Y-27632, or HA1077, blunted renal microvascular vasoconstriction to the ETB receptor agonist, IRL-1620, to the A1 agonist, cyclopentylThe costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Address for reprint requests and other correspondence: E. W. Inscho, Dept. of Physiology, Medical College of Georgia, 1120 15th St., Augusta, GA 30912-3000 (e-mail: F590
0363-6127/09 $8.00 Copyright 2009 the American Physiological Society
adenosine, or to guanylyl cyclase inhibition. Myogenic responses are blunted by Rho-kinase inhibition in hydronephrotic kidneys and in nonrenal blood vessels (50, 62). The effects on autoregulation in intact kidneys or the P2 receptor events postulated to participate in autoregulatory responses have not been investigated. Therefore, the current study was undertaken to assess the impact of Rho-kinase inhibition on pressure-mediated autoregulatory behavior and on the vasoconstriction induced by P2 receptor agonists.


Studies were approved by the Committee on Animal Use for Research and Education at the Medical College of Georgia. Juxtamedullary nephron preparation. Experiments were performed in vitro using kidneys prepared for the blood-perfused juxtamedullary nephron technique, as previously described (25, 29). Ninety-eight male Sprague-Dawley rats (g) were used to complete these studies. For each experiment, two animals were anesthetized with pentobarbital sodium (40 mg/kg ip) and prepared for videomicroscopy experiments. Perfusate blood was collected and prepared, as previously described (28, 29). Briey, blood was collected from the nephrectomized blood donor rat into a heparinized syringe (500 U). The plasma and washed erythrocyte fractions were combined to yield a reconstituted blood perfusate with a hematocrit of 33% as previously described (25, 29). When the dissection was completed, the Tyrodes buffer perfusate was replaced with the reconstituted blood. The blood perfusate was stirred continuously in a closed reservoir while being oxygenated with a 95% O2-5% CO2 gas mixture. Perfusion pressure was continuously monitored using a pressure cannula positioned in the tip of a doublebarreled perfusion cannula and connected to a pressure transducer (model TRN005, Kent Scientic) linked to a Grass Polygraph (model 7D, Grass Instrument, Quincy, MA). Perfusion pressure was xed at 110 mmHg. The inner cortical surface of the kidney was superfused with Tyrodes buffer (37C) containing 1.0% bovine serum albumin and the kidney was allowed to equilibrate for at least 15 min. The perfusion chamber, containing the prepared kidney, was attached to the stage of a Nikon Optiphot-2UD microscope (Nikon, Tokyo, Japan) equipped with a Zeiss water immersion objective (40). The tissue was transilluminated and the focused image, obtained with a Newvicon camera (NC-70, Dage-MTI, Michigan City, IN), was passed through an image processor (MFJ-1425, MFJ Enterprises, Starkville, MS) and displayed on a video monitor while being simultaneously recorded on DVD for later analysis. Vascular inside diameters were measured at a single site using an image shearing monitor (model 908, Vista Electronics, Ramona, CA). The image shearing monitor was calibrated using a stage micrometer. Experimental protocols. Afferent arteriolar responses were determined to changes in renal perfusion pressure, or administration of vasoactive agonists and antagonists. Autoregulatory behavior was assessed by measuring changes in afferent arteriolar diameter in response to acute elevations in renal perfusion pressure. Measurements of afferent arteriolar diameter were made continuously at 12-s intervals. Sustained afferent arteriolar diameter was calculated from the average of all measurements made during the nal 2 min of each treatment period. Each protocol began with a 5-min control period to ensure a stable vessel diameter and was followed by either agonist stimulation or an increase in renal perfusion pressure to establish the control response. Effect of Y-27632 on afferent arteriolar responses to angiotensin II and to acute increases in renal perfusion pressure. The effect of angiotensin II, and of increasing renal perfusion pressure, on afferent arteriolar diameter was determined with and without treatment with the Rho-kinase inhibitor, Y-27632 (3, 13, 14, 65). Experiments examined afferent arteriolar responses to 1.0 nM angiotensin II

AJP-Renal Physiol VOL

followed by introduction of Y-27632 at concentrations of 0.1, 1.0, and 10 M for a period of 20 min. In the presence of Y-27632, afferent arteriolar autoregulatory responses were measured at perfusion pressures of 100, 65, 130, and 160 mmHg and again at 100 mmHg in successive 5-min periods, followed by reassessment of the response to angiotensin II. Separate control animals were prepared to establish afferent arteriolar autoregulatory responses and responses to angiotensin II in naive controls. Separate groups of rats were used for each concentration of Y-27632. Y-27632 and angiotensin II were applied in the superfusion solution. Effect of Y-27632 on the afferent arteriolar response to P2 receptor agonists, ATP, , -methylene ATP, and UTP. P2 receptors are important for afferent arteriolar autoregulatory responses. Thus, experiments were performed to determine the effect of Rho-kinase inhibition with Y-27632 on the vasoconstriction induced by P2 receptor activation. Renal microvessels express P2X1 and P2Y2 receptors, which are activated by ATP. P2X1 receptors have been implicated in mediating afferent arteriolar autoregulatory responses. Accordingly, we examined the impact of Rho-kinase inhibition on the vasoconstrictor actions of the P2X1 agonist, , -methylene ATP, the P2Y2 agonist, UTP, and the endogenous ligand for P2 receptors, ATP. Afferent arteriolar responses were determined before and during Y-27632 (1.0 M) treatment. Western blot analysis of renal cortex, renal medulla, and the preglomerular microvasculature. Renal cortex, medulla, and freshly isolated preglomerular microvessels were homogenized in an ice-cold homogenization buffer containing 50 mM Tris, pH 7.4, 150 mM NaCl, 1% NP-40, 0.25% deoxycholic acid, 1.0 mM EDTA, and supplemented with 1 mM phenylmethylsulfornyl uoride, 1.0 mM Na3VO4, and 1 protease inhibitor cocktail. After the tissue lysates were centrifuged (10,000 g; 30 min), the supernatants were collected and protein concentrations were determined by a bicinchoninic acid kit. Lanes were loaded with equal amounts of total protein and the individual proteins were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and subsequently transferred to nitrocellulose membrane. Membranes were blocked for 1 h with 5% milk in Tris-buffered saline containing 0.5% Tween-20 (TBST) and then incubated with monoclonal antibody, Rho-kinase (1:1,000), or Rho-kinase (1:1,000) overnight at 4C. After being washed with TBST, the membranes were incubated with a horseradish peroxidaselinked secondary antibody and visualized using an enhanced chemiluminescence kit. Statistical analysis. Data were evaluated using a one-way ANOVA for repeated measures. Differences between group means, within each series, were determined using Newman-Kuels multiple range test. P values 0.05 were considered to indicate statistically signicant differences. All values are reported as means SE. Materials. Male Sprague-Dawley rats were obtained from Charles River Laboratories (Raleigh, NC). Bovine serum albumin and Y-27632 were obtained from Calbiochem (La Jolla, CA). Bicinchoninic acid protein assay kit was purchased from Pierce (Rockford, IL). Chemiluminescence kit was purchased from Amersham (Piscataway, NJ). Protease inhibitor cocktail was purchased from Roche Applied Science (Indianapolis, IN). Rho-kinase and Rho-kinase antibodies were purchased from BD Biosciences (San Jose, CA). All other reagents were purchased from Sigma (St. Louis, MO).


Initial experiments determined the effect of Y-27632 on pressure-mediated autoregulatory responses and on the afferent arteriolar response to angiotensin II. Under control conditions, at 100 mmHg, afferent arteriolar diameter averaged 15.9 0.7 m (n 15) and was similar across the three Y-27632 treatment groups. In the absence of Y-27632, exposure to 1.0 nM angiotensin II reduced afferent arteriolar diameter similarly by 14 4, 18 2, and 16 2% (n 5, P 0.05 vs. control

296 MARCH 2009
in each Y-27632 group), respectively (Fig. 1, left). In the presence of Y-27632, baseline vessel diameter increased in a concentration-dependent manner. Afferent arteriolar diameter increased by 10 4, 22 3, and 43 7% in response to 100 nM, 1.0 M, and 10 M Y-27632 concentrations, respectively. Y-27632 treatment inhibited angiotensin II-mediated vasoconstriction at concentrations above 100 nM (Fig. 1, right). Exposure to 1.0 nM angiotensin II reduced afferent arteriolar diameter by and 6 2% at Y-27632 concentrations of 100 nM and 1.0 M and eliminated the response at the 10 M Y-27632 concentration. Compared with control arterioles (Fig. 2, black circles), autoregulatory responsiveness was attenuated at each Y-27632 concentration examined (Fig. 2, square symbols). Signicant pressure-mediated autoregulatory responses were observed in
Fig. 2. Increasing concentrations of Y-27632 inhibit the pressure-mediated afferent arteriolar autoregulatory response. Data are plotted as a percent of the control diameter. Control arterioles are depicted by black circles. Data from arterioles treated with Y-27632 are depicted by square symbols (0.1 M Y-27632, white squares; 1 M Y-27632, gray squares; and 10 M Y-27632, black squares). The sample size for each group is indicated by numbers in parentheses. *P 0.05 vs. diameter at 100 mmHg. #P 0.05 vs. control diameter before Y-27632 treatment.
Fig. 1. Increasing concentrations of Y-27632 inhibit the afferent arteriole response to angiotensin II (ANG II). Responses before (left) and during (right) treatment with Y-27632 are depicted. Y-27632 was administered at concentrations of 100 nM (bottom), 1 M (middle), and 10 M (top). Responses of individual arterioles are depicted by the plots (gray circle symbols) and mean responses are depicted by the black squares. *P 0.05 vs. the diameter before ANG II treatment. #P 0.05 vs. the response ANG II before Y-27632 treatment. The P values presented in each gure represent comparison of the response before and during Y-27632 treatment; n 5 in each Y-27632 treatment group. Con, control. AJP-Renal Physiol VOL
arterioles treated with 0.1 M Y-27632 (white squares) but higher concentrations of Y-27632 virtually eliminated the autoregulatory response resulting in either a at pressure diameter relationship (1.0 M, gray squares) or a pressuredependent increase in diameter consistent with a passive pressure diameter relationship (10 M, black squares). These data suggest that Rho-kinase plays an important role in pressuremediated autoregulatory vasoconstriction. In separate experiments, we determined the effect of Y-27632 on the afferent arteriolar response to P2 receptor activation. Control diameters were similar across treatment groups and averaged 17.7 1.1, 17.7 0.6, and 16.5 0.6 m for the 1.0, 10, and 100 M ATP groups, respectively. As shown in Fig. 3, left, ATP produced a signicant and reversible afferent arteriolar vasoconstriction. Afferent diameter decreased by 13, 25, and 23% in response to 1, 10, and 100 M ATP, respectively. Y-27632 blunted the afferent arteriolar response to ATP (Fig. 3, right). In the presence of Y-27632, afferent diameter decreased by 5, 15, and 7% in response to 1, 10, and 100 M ATP, respectively. While 10 M ATP still reduced diameter signicantly, the magnitude of the vasoconstriction evoked by each ATP concentration was signicantly reduced compared with the control responses in the absence of Y-27632. Renal microvessels express multiple P2 receptor subtypes including P2X1 and P2Y2 (25, 29, 32, 67, 69). P2X1 receptors, but not P2Y2 receptors, have been implicated in mediating pressure-dependent autoregulatory responses of afferent arterioles (27, 30). Given that Y-27632 signicantly inhibited autoregulatory responses, we examined the effect of Y-27632 of afferent arteriolar response to P2X1 and P2Y2 receptor activation. P2X1 receptors were stimulated using the selective agonist, , -methylene ATP (1.0 M), whereas UTP (10 M) was used to selectively stimulate P2Y2 receptors (56). These concentrations were selected based on previous studies showing that they yield vasoconstrictor responses similar in magnitude to those obtained with ATP (29). As shown in Fig. 4, left, , -methylene ATP (bottom) and UTP (top) signicantly and reversibly reduced afferent arteriolar diameter by and

ATP and , -methylene ATP are biphasic with a rapid initial phase that partially recovers to a stable diameter smaller than the control diameter (Fig. 5, bottom and middle). Responses to UTP and other P2Y2 agonists are monophasic in that diameter decreases rapidly on exposure to agonists but vessel diameter quickly stabilizes at or near its nadir (Fig. 5). Baseline diameter increased signicantly on introduction of Y-27632 to the bathing solution. Y-27632 had no detectable effect on the rapid initial response evoked by , -methylene ATP but the sustained vasoconstriction was completely eliminated (Fig. 5, bottom). Similarly, the initial phase of the response to ATP was also unaffected by Y-27632 but the magnitude of the sustained vasoconstriction was signicantly blunted compared with the control condition. Interestingly, the time course and magnitude of the response evoked by UTP during Y-27632 treatment were similar to the control conditions. These data support the contention that different signaling pathways are involved in P2X vs. P2Y receptor activation and that Rho-kinase plays unique roles in those pathways. Figure 6 presents representative Western blots demonstrating expression of Rho-kinase isoforms in homogenates of preglomerular microvessels, renal cortex, and renal medulla. -Actin staining is provided as a loading control. Clearly,
Fig. 3. Y-27632 inhibits afferent arteriolar responses to increasing concentrations of ATP. The afferent arteriolar response to ATP (1.0 M, bottom; 10 M, middle; and 100 M, top) was determined before (left) and during (right) treatment with 1 M Y-27632. Responses of individual arterioles are depicted by the gray symbols and the mean responses are presented by the black squares. *P 0.05 vs. control diameter before ATP exposure. #P 0.05 vs. magnitude of the control response before Y-27632 treatment.
31 5%, respectively. In the presence of Y-27632, the sustained response to , -methylene ATP was completely eliminated while the response to UTP was not signicantly affected. These data suggest that Rho-kinase may exert differential inuences on vasoconstrictor signals evoked by P2X receptors compared with those elicited by P2Y receptor activation. The data plotted in Fig. 5 provide a temporal prole of the vasoconstriction evoked by , -methylene ATP (1.0 M; bottom), ATP (10 M; middle), and UTP (10 M; top) before and during treatment with Y-27632. Consistent with previous reports (29, 30), afferent arteriolar vasoconstrictor responses to
Fig. 4. Y-27632 inhibits the afferent arteriolar response to P2X1 receptor stimulation, but not P2Y2 receptor activation. P2X1 receptors were stimulated with , -methylene ATP (1.0 M, bottom) and P2Y2 receptors were stimulated with UTP (10 M, top). Control responses are shown on the left and responses during Y-27632 treatment are shown on the right. Responses of individual arterioles are depicted by the gray symbols and the mean responses are presented by the black squares. *P 0.05 vs. control diameter before agonist exposure. #P 0.05 vs. magnitude of the control response before Y-27632 treatment.

Fig. 5. Temporal response afferent arterioles to P2 receptor agonists before and during Y-27632 treatment. Control responses are depicted by the black symbols and responses obtained from the same arterioles during Y-27632 treatment are depicted by the white symbols. Responses obtained with UTP, ATP, and , -methylene ATP are presented in the top, middle, and bottom, respectively. Each symbol represents measurements taken at 12-s intervals. The response during Y-27632 administration is overlaid on the control response for comparison. *P 0.05 vs. control diameter at 100 mmHg. #P 0.05 vs. the diameter in the absence of Y-27632.
tory responses and in responses to autoregulatory mediators (50). Western blot analysis demonstrated preglomerular expression of Rho-kinase and Rho-kinase as well as expression in renal cortical and medullary homogenates. The Rhokinase inhibitor blunted or abolished afferent arteriolar responses to angiotensin II and selected P2 receptor agonists while having little effect on other P2 receptor activators. Importantly, the Rho-kinase inhibitor signicantly attenuated pressure-mediated autoregulatory behavior suggesting that Rho-kinase is an important part of the renal microvascular myogenic signaling cascade. Consistent with previous reports, Y-27632 signicantly blunted afferent arteriolar vasoconstriction mediated by angiotensin II (13, 14). The magnitude of the inhibition increased as Y-27632 concentration increased from 100 nM to 10 M. It is known that angiotensin II induces vasoconstriction of afferent arterioles by stimulating calcium inux through L-type calcium channels and by stimulating calcium release from intracellular stores (11, 18, 20, 24, 36, 46, 63, 64, 68, 71). Based on our ndings, and those of others, it is now clear that a portion of the vasoconstriction induced by angiotensin II involves activation of Rho-kinase and presumably enhanced calcium sensitivity (13, 14). Autoregulation is a critical function of afferent arterioles (37, 44, 51, 53, 61). Setting preglomerular resistance appropriately is essential for maintenance of a stable renal blood ow and glomerular ltration rate. Autoregulatory adjustments in resistance are calcium dependent and, like the angiotensin II responses, they involve both voltage-dependent calcium inux and calcium mobilization from intracellular stores (4, 12, 22, 28, 49, 52, 58). In the current study, the Rho-kinase inhibitor Y-27632 evoked a concentration-dependent increase of baseline diameter and a concentration-dependent inhibition of pressuremediated vasoconstriction of juxtamedullary afferent arterioles. At the highest concentration tested, increasing perfusion pressure from 65 to 160 mmHg resulted in a pressure-dependent increase in diameter consistent with a passive pressure/ diameter relationship. This blunting of autoregulatory behavior was apparent at each pressure step tested and is consistent with the ndings of Nakamura et al. (50) who also reported blunted pressure-dependent responses in the hydronephrotic kidney. Therefore, Rho-kinase activity is an important part of the

Rho-kinase (180 kDa) and Rho-kinase (160 kDa) were also detected in the preglomerular microvasculature, renal cortex, and renal medulla, thus supporting the functional data provided in Figs. 15, which implicate Rho-kinase in renal vascular function.


The current report establishes a central role for Rho-kinase in regulating afferent arteriolar function and extends previous work to demonstrate Rho-kinase involvement in autoregulaAJP-Renal Physiol VOL
Fig. 6. Expression of Rho-kinase isoforms in rat preglomerular microvessels (MV), renal cortex (C), and renal medulla (M). Prominent bands are detected for Rho-kinase at 180 kDa and Rho-kinase at 160 kDa.
tension-generating machinery responsible for autoregulatory behavior. In the kidney, complete autoregulatory responses reect the combined inuences of tubuloglomerular feedback and the myogenic mechanism (51, 53). The inhibition observed in this report likely represents inhibition of myogenic responses as the diameter measurements were made in the rst half of afferent arteriolar length (4752% of the arterioles length), well removed from the tubuloglomerular feedback-sensitive region. This conclusion is also supported by similar observations made in the hydronephrotic kidney, which is devoid of tubuloglomerular feedback inuences (50). In addition, inhibition of myogenic behavior has also been reported for other vascular smooth muscle tissues, thus indicating that Rho-kinase involvement in myogenic behavior is not restricted to the renal microcirculation and may represent a common feature of myogenic control systems (17, 57, 62). Autoregulatory resistance adjustments are induced by activation of ATP-sensitive P2 receptors (26, 30, 47). This is a large receptor class made up of two distinct receptor families, P2X and P2Y (56). This classication is based on important structural differences and mechanistic differences in the intracellular signal transduction pathways utilized. The ionotropic P2X receptor family includes seven unique receptor subtypes labeled P2X1 through P2X7 (55). P2X receptors are membranebound ligand-gated ion channels composed of two transmembrane domains coupled to a large extracellular loop and short intracellular tails (55). Receptor activation opens the ligandgated channel permitting inux of a nonselective cation current producing a rapid and reversible vasoconstriction (5, 25, 55, 67). P2Y receptors are metabotropic, membrane-bound receptors with seven membrane-spanning domains and currently include approximately eight subtypes (P2Y1, P2Y2, P2Y4, P2Y6, P2Y11, P2Y12, P2Y13, and P2Y14) (1, 7, 56). P2Y receptor activation can produce either vasoconstriction or vasodilation. P2Y receptors expressed by vascular smooth muscle stimulate vasoconstriction by increasing intracellular calcium concentration and/or by activating the Rho-kinase pathway (15, 25, 32, 54, 59). Based on a collection of evidence, it appears that afferent arterioles express P2X1 and P2Y2 receptors at a minimum, and we provided considerable evidence that P2X1 receptors are essential for transducing increases in perfusion pressure into autoregulatory afferent arteriolar vasoconstrictor responses (26, 29, 32, 67, 69). Because Rho-kinase inhibition blunts autoregulatory behavior, we examined the impact of Y-27632 on the afferent arteriolar response to ATP and to selective activation of P2X1 receptors (, -methylene ATP) and P2Y2 receptors (UTP). As noted in the current study, Y-27632 completely blocked the sustained vasoconstriction induced by P2X1 receptor activation and by 1.0 M ATP. In contrast, Y-27632 inhibition had little impact on the sustained vasoconstriction induced by P2Y2 receptor activation with UTP. Previous studies showed that afferent arteriolar responses to lower concentrations of ATP (1.0 M) were calcium inux dependent and could be completely blocked by L-type calcium channel blockade (25, 32). Virtually identical results were obtained during P2X1 receptor activation suggesting that lower ATP concentrations induce their effects primarily through P2X1 receptor activation. Higher concentrations of ATP induce vasoconstriction through

mechanisms driven more by calcium mobilization, and these responses are mimicked by the P2Y2 agonist UTP. These observations suggest that responses to higher ATP concentrations involve both P2X1 and P2Y2 receptor activation. In the current report, Y-27632 treatment signicantly attenuated ATP-mediated vasoconstriction at all ATP concentrations tested. Given that ATP is capable of activating both P2X and P2Y receptors and that these receptors evoke vasoconstriction through disparate calcium signaling mechanisms, it is possible that retention of some vasoconstrictor activity could reect this dual receptor activation. The exact explanation for this observation remains unclear. Nevertheless, the results reecting markedly different outcomes using the P2X1 and P2Y2 agonists argue that Rho-kinase exerts complex regulatory inuences in the renal microcirculation. Thus, Rho-kinase activation is more than just a nal common pathway linking vasoconstrictor stimuli to vasoconstrictor events. Indeed, afferent arterioles employ Rho-kinase activation as an essential component of the signaling pathway for some but not all vasoconstrictor agonists. These data demonstrate that Rhokinase activation is an important part of the intracellular signaling mechanisms that connect P2X1 receptor activation with vasoconstriction. In addition, these data demonstrate Rhokinase-dependent contractile events link P2X1 receptor activation with autoregulatory adjustments in renal vascular resistance. Typical ATP-mediated vasoconstrictions are biphasic and manifest as a rapid initial vasoconstriction followed by a partial recovery until a sustained constriction diameter is reached. It is important to note that Y-27632 had little effect on the rapid initial vasoconstriction while having more pronounced effects on the sustained vasoconstriction. The explanation for these distinct temporal effects is unclear. Perhaps Rho-kinase is essential for the sustained response to receptor activation rather than participating in the initiating event arising from receptor activation. The refractory nature of this rapid initial vasoconstriction has been observed previously (33, 70). Calcium channel blockade, or inhibition of 20-HETE, did not affect this initial contractile event substantially, while completely blocking the sustained vasoconstriction. Interestingly, reducing the extracellular calcium concentration (200 nM) eliminated both the initial and the sustained vasoconstriction induced by P2X1 receptor activation (33). These data indicate that calcium inux is important for both aspects on the biphasic vasoconstriction by P2X1 receptors. Thus, the initial vasoconstriction may largely reect the inwardly directed, nonselective cation current that begins immediately on agonist activation of the ligand-gated P2X1 receptor protein. The inhibitor data provide functional evidence that Rhokinase participates in the generation and maintenance of active tension in afferent arteriolar smooth muscle. We used Western blot analysis to demonstrate the presence of Rho-kinase isoforms in freshly isolated preglomerular microvessels, to demonstrate that the enzyme target was present, and to support the concept that Rho-kinase activation exerts important functional effects. Preglomerular microvessels as well as the renal cortex and renal medulla clearly express Rho-kinase and. Together, these proteins make up important elements of the Rho-signaling pathway and support the argument that inhibition of autoregulatory behavior and P2X1 receptor-mediated vasoconstriction by Y-27632 occurs through inhibition of the

Rho-KINASE IN THE RENAL MICROCIRCULATION 15. Chaulet H, Desgranges C, Renault MA, Dupuch F, Ezan G, Peiretti F, Loirand G, Pacaud P, Gadeau AP. Extracellular nucleotides induce arterial smooth muscle cell migration via osteopontin. Circ Res 89: 772778, 2001. 16. Chitaley K, Weber D, Webb RC. RhoA/Rho-kinase, vascular changes, and hypertension. Curr Hypertens Rep 3: 139 144, 2001. 17. Cipolla MJ, Gokina NI, Osol G. Pressure-induced actin polymerization in vascular smooth muscle as a mechanism underlying myogenic behavior. FASEB J 16: 7276, 2002. 18. Conger JD, Falk SA. KCl and angiotensin responses in isolated rat renal arterioles: effects of diltiazem and low-calcium medium. Am J Physiol Renal Fluid Electrolyte Physiol 264: F134 F140, 1993. 19. Conger JD, Falk SA, Robinette JB. Angiotensin II-induced changes in smooth muscle calcium in rat renal arterioles. J Am Soc Nephrol 3: 17921803, 1993. 20. Gonzalez E, Salomonsson M, Kornfeld M, Gutierrez AM, Morsing P, Persson AEG. Different action of angiotensin II and noradrenaline on cytosolic calcium concentration in isolated and perfused afferent arterioles. Acta Physiol Scand 145: 299 300, 1992. 21. Grifn KA, Picken M, Bakris GL, Bidani AK. Comparative effects of selective T- and L-type calcium channel blockers in the remnant kidney model. Hypertension 37: 1268 1272, 2001. 22. Hayashi K, Epstein M, Loutzenhiser R. Pressure-induced vasoconstriction of renal microvessels in normotensive and hypertensive rats: studies in the isolated perfused hydronephrotic kidney. Circ Res 65: 14751484, 1989. 23. Huang C, Davis G, Johns EJ. Effect of nitrendipine on autoregulation of perfusion in the cortex and papilla of kidneys from Wistar and stroke prone spontaneously hypertensive rats. Br J Pharmacol 111: 111116, 1994. 24. Imig JD, Cook AK, Inscho EW. Postglomerular vasoconstriction to angiotensin and norepinephrine depend on release of Ca2 from intracellular stores. Gen Pharmacol 34: 409 415, 2001. 25. Inscho EW, Cook AK. P2 receptor-mediated afferent arteriolar vasoconstriction during calcium channel blockade. Am J Physiol Renal Physiol 282: F245F255, 2002. 26. Inscho EW, Cook AK, Imig JD, Vial C, Evans RJ. Physiological role for P2X1 receptors in renal microvascular autoregulatory behavior. J Clin Invest 112: 18951905, 2003. 27. Inscho EW, Cook AK, Imig JD, Vial C, Evans RJ. Renal autoregulation in P2X1 knockout mice. Acta Physiol Scand 181: 445 453, 2004. 28. Inscho EW, Cook AK, Mui V, Imig JD. Calcium mobilization contributes to pressure-mediated afferent arteriolar vasoconstriction. Hypertension 31: 421 428, 1998. 29. Inscho EW, Cook AK, Mui V, Miller J. Direct assessment of renal microvascular responses to P2-purinoceptor agonists. Am J Physiol Renal Physiol 274: F718 F727, 1998. 30. Inscho EW, Cook AK, Navar LG. Pressure-mediated vasoconstriction of juxtamedullary afferent arterioles involves P2-purinoceptor activation. Am J Physiol Renal Fluid Electrolyte Physiol 271: F1077F1085, 1996. 31. Inscho EW, Imig JD, Cook AK. Afferent and efferent arteriolar vasoconstriction to angiotensin II and norepinephrine involves release of Ca2 from intracellular stores. Hypertension 29: 222227, 1997. 32. Inscho EW, LeBlanc EA, Pham BT, White SM, Imig JD. Purinoceptormediated calcium signaling in preglomerular smooth muscle cells. Hypertension 33: 195200, 1999. 33. Inscho EW, Ohishi K, Cook AK, Belott TP, Navar LG. Calcium activation mechanisms in the renal microvascular response to extracellular ATP. Am J Physiol Renal Fluid Electrolyte Physiol 268: F876 F884, 1995. 34. Inscho EW, Schroeder AC, Deichmann PC, Imig JD. ATP-mediated Ca2 signaling in preglomerular smooth muscle cells. Am J Physiol Renal Physiol 276: F450 F456, 1999. 35. Ito S, Kume H, Honjo H, Katoh H, Kodama I, Yamaki K, Hayashi H. Possible involvement of Rho kinase in Ca2 sensitization and mobilization by MCh in tracheal smooth muscle. Am J Physiol Lung Cell Mol Physiol 280: L1218 L1224, 2001. 36. Iversen BM, Arendshorst WJ. ANG II and vasopressin stimulate calcium entry in dispersed smooth muscle cells of preglomerular arterioles. Am J Physiol Renal Physiol 274: F498 F508, 1998. 37. Just A. Mechanisms of renal blood ow autoregulation: dynamics and contributions. Am J Physiol Regul Integr Comp Physiol 292: R1R17, 2007.

Rho-kinase pathway. Abundant expression is also noted in the renal cortex and the renal medulla suggesting important roles for the Rho-kinase system in tubular function or in other vascular tissues in these kidney regions. In summary, we conrmed previous reports from hydronephrotic kidney preparations that Rho-kinase contributes to angiotensin II- and pressure-mediated vasoconstriction of afferent arterioles (14, 50). The results of the current report extend the previous ndings in several ways. The impact of Rho-kinase inhibition on autoregulatory behavior has been demonstrated in a renal preparation possessing normal vascular circuitry and an intact tubular system. In addition, we showed that the autoregulatory impairment coincides with similar impairment of autoregulatory P2X1 receptor signaling, which is distinct from P2Y receptor-mediated effects.
GRANTS This work was supported by grants from the American Heart Association (AHA; 95001370) and the National Institutes of Health (DK-44628, DK38226). E. W. Inscho was an Established Investigator of the AHA during portions of this study. Present address of Dr. L.-M. Jin: Dept. of Internal Medicine, Div. of Endocrinology, Clinical Nutrition and Vascular Medicine, Univ. of California, Davis, CA 95616. REFERENCES 1. Abbracchio MP, Burnstock G, Boeynaems JM, Barnard EA, Boyer JL, Kennedy C, Knight GE, Fumagalli L, Gachet C, Jacobson KA, Weisman GA. International Union of Pharmacology LVIII: update on the P2Y G protein-coupled nucleotide receptors: from molecular mechanisms and pathophysiology to therapy. Pharmacol Rev 58: 281341, 2006. 2. Amano M, Ito M, Kimura K, Fukata Y, Chihara K, Nakano T, Matsuura Y, Kaibuchi K. Phosphorylation and activation of myosin by Rho-associated kinase (Rho-kinase). J Biol Chem 271: 20246, 1996. 3. Batchelor TJP, Sadaba JR, Ishola A, Pacaud P, Munsch CM, Beech DJ. Rho-kinase inhibitors prevent agonist-induced vasospasm in human internal mammary artery. Br J Pharmacol 132: 302308, 2001. 4. Bell PD. Calcium antagonists and intrarenal regulation of glomerular ltration rate. Am J Nephrol 7: 24 31, 1987. 5. Boeynaems JM, Communi D, Gonzalez NS, Robaye B. Overview of the P2 receptors. Semin Thromb Hemost 31: 139 149, 2005. 6. Bolz SS, Vogel L, Sollinger D, Derwand R, De Wit C, Loirand G, Pohl U. Nitric oxide-induced decrease in calcium sensitivity of resistance arteries is attributable to activation of the myosin light chain phosphatase and antagonized by the RhoA/Rho kinase pathway. Circulation 107: 3081, 2003. 7. Burnstock G. Purinergic signalling. Br J Pharmacol 147: S172S181, 2006. 8. Carmines PK, Fowler BC, Bell PD. Segmentally distinct effects of depolarization on intracellular [Ca2] in renal arterioles. Am J Physiol Renal Fluid Electrolyte Physiol 265: F677F685, 1993. 9. Carmines PK, Inscho EW, Gensure RC. Arterial pressure effects on preglomerular microvasculature of juxtamedullary nephrons. Am J Physiol Renal Fluid Electrolyte Physiol 258: F94 F102, 1990. 10. Carmines PK, Mitchell KD, Navar LG. Effects of calcium antagonists on renal hemodynamics and glomerular function. Kidney Int 41, Suppl 36: S43S48, 1992. 11. Carmines PK, Navar LG. Disparate effects of Ca channel blockade on afferent and efferent arteriolar responses to ANG II. Am J Physiol Renal Fluid Electrolyte Physiol 256: F1015F1020, 1989. 12. Casellas D, Carmines PK. Control of the renal microcirculation: cellular and integrative perspectives. Curr Opin Nephrol Hypertens 5: 57 63, 1996. 13. Cavarape A, Bauer J, Bartoli E, Endlich K, Parekh N. Effects of angiotensin II, arginine vasopressin and tromboxane A2 in renal vascular bed: role of rho-kinase. Nephrol Dial Transplant 18: 1764 1769, 2003. 14. Cavarape A, Endlich N, Assaloni R, Bartoli E, Steinhausen M, Parekh N, Endlich K. Rho-kinase inhibition blunts renal vasoconstriction induced by distinct signaling pathways in vivo. J Am Soc Nephrol 14: 37 45, 2003. AJP-Renal Physiol VOL

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54. Nishiyama A, Rahman M, Inscho EW. Role of interstitial ATP and adenosine in the regulation of renal hemodynamics and microvascular function. Hypertens Res 27: 791 804, 2004. 55. North RA, Surprenant A. Pharmacology of cloned P2X receptors. Annu Rev Pharmacol Toxicol 40: 563580, 2000. 56. Ralevic V, Burnstock G. Receptors for purines and pyrimidines. Pharmacol Rev 50: 413 492, 1998. 57. Randriamboavonjy V, Busse R, Fleming I. 20-HETE-induced contraction of small coronary arteries depends on the activation of rho-kinase. Hypertension 41: 801 806, 2003. 58. Sanchez-Ferrer CF, Roman RJ, Harder DR. Pressure-dependent contraction of rat juxtamedullary afferent arterioles. Circ Res 64: 790 798, 1989. 59. Sauzeau V, Le Jeune H, Cario-Toumaniantz C, Vaillant N, Gadeau AP, Desgranges C, Scalbert E, Chardin P, Pacaud P, Loirand G. P2Y1, P2Y2, P2Y4, and P2Y6 receptors are coupled to Rho and Rho kinase activation in vascular myocytes. Am J Physiol Heart Circ Physiol 278: H1751H1761, 2000. 60. Savineau JP, Marthan R. Modulation of the calcium sensitivity of the smooth muscle contractile apparatus: molecular mechanisms, pharmacological and pathophysiological implications. Fundam Clin Pharmacol 11: 289 299, 1997. 61. Schnermann J, Levine DZ. Paracrine factors in tubuloglomerular feedback: adenosine, ATP and nitric oxide. Annu Rev Physiol 65: 501529, 2003. 62. Schubert R, Kalentchuk VU, Krien U. Rho kinase inhibition partly weakens myogenic reactivity in rat small arteries by changing calcium sensitivity. Am J Physiol Heart Circ Physiol 283: H2288 H2295, 2002. 63. Takahara A, Suzuki-Kusaba M, Hisa H, Satoh S. Effects of a novel Ca2 entry blocker, CD-349, and TMB-8 on renal vasoconstriction induced by angiotensin II and vasopressin in dogs. J Cardiovasc Pharmacol 16: 966 970, 1990. 64. Takenaka T, Forster H, Epstein M. Protein kinase C and calcium channel activation as determinants of renal vasoconstriction by angiotensin II and endothelin. Circ Res 73: 743750, 1993. 65. Uehata M, Ishizaki T, Satoh H, Ono T, Kawahara T, Morishita T, Tamakawa H, Yamagami K, Inui J, Maekawa M, Narumiya S. Calcium sensitization of smooth muscle mediated by a Rho-associated protein kinase in hypertension. Nature 389: 990 994, 1997. 66. VanBavel E, Wesselman JPM, Spaan JAE. Myogenic activation and calcium sensitivity of cannulated rat mesenteric small arteries. Circ Res 82: 210 220, 1998. 67. White SM, Imig JD, Inscho EW. Calcium signaling pathways utilized by P2X receptors in preglomerular vascular smooth muscle cells. Am J Physiol Renal Physiol 280: F1054 F1061, 2001. 68. Yiu SS, Zhao X, Inscho EW, Imig JD. 12-Hydroxyeicosatetraenoic acid participates in angiotensin II afferent arteriolar vasoconstriction by activating L-type calcium channels. J Lipid Res 44: 23912399, 2003. 69. Zhao X, Cook AK, Field M, Edwards B, Zhang S, Zhang Z, Pollock JS, Imig JD, Inscho EW. Impaired Ca2 signaling attenuates P2X receptor-mediated vasoconstriction of afferent arterioles in angiotensin II hypertension. Hypertension 46: 562568, 2005. 70. Zhao XY, Inscho EW, Bondlela M, Falck JR, Imig JD. The CYP450 hydroxylase pathway contributes to P2X receptor-mediated afferent arteriolar vasoconstriction. Am J Physiol Heart Circ Physiol 281: H2089 H2096, 2001. 71. Zhu ZM, Arendshorst WJ. Angiotensin II receptor stimulation of cytosolic calcium concentration in cultured renal resistance arterioles. Am J Physiol Renal Fluid Electrolyte Physiol 271: F1239 F1247, 1996.



Arianne T 2100.2599 T 2615, 2620, 2621 T 2740, 2760 Discovery T 6060, 6072, 6750, 6810 Freemotion TFB 2011, 2112, 2223, 2242, 2283 TSE 0100 Micropower SC 100, 115, 120, 125 SC 145, 150, 155 Microspace SCT 30, 35, 45, 46, 48 Octopus TBO 230 Pure Power TGP 1410 TPP 2010, 2020, 2205, 2210,2310, 2320 Sensory Cyclonic TC 5208, 5228 Sensory TFS 2350 TS 1613.1625 TS 1723.1726 TS 1823.1873 TS 1942.1983 TS 2024.2079 TS 2164.2171 TS 2264.2277 TS 2344, 2350, 2356, 2358, 2360, 2366, 2375, 2394 Silent Energy TSE 0100, 0135 Telios Cyclonic TC 2885, 3206 Telios T 4300.4599 T 5400.5899 TP 6210, 6214, 6216 Original: H 60, 61


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P 3502 P 1770 P 1770 P P P 2585 P P 4095 E 53 48

DT 1200 ETA 405

P P P 5801 P 1985 P 3502 P P 2585 P 3502 P 3502 P 5801 P P 1770 P 5801 P 2700 P 2700 P

BS 250 BS 960


DAA 039



Domatic : 1500

STB 1400 STB 4000

BS 850 BS 1290E HSS 750


EBS 1400 EBS 1401


E 952 K 029 ST 017 ST 018


Radel XTC 15E XD 100 ED XD 1000/ MD/ PD/ PS/ SD XTC 1200, 1300E, 1400E XTJ 140 B XTRC 140E XW 1200, 1200 PS Cleos : XTH 170, 180 EW Compacto : XTC 12, 13/ E, 14/ E/ PC, 15E Darel : XTC, XTCN Darel : XWDA 150 Domo Compact : XS 1100 D, Metal 1100 Floor Line : XT 1200, 1300/E Floor Line : XTE 1200 E, 1300 E Floor Line : XTR 1300 M 31 : Penta Maximum : XTL 130 E, 135 E Maximum : XTL 140 E/ EX 3, 145 E Maximum : XTL 150 E/ EX 3 Orbit : XTA 3080 E Orbit : XTD 3070 E, 3080 E, 3090 E, 3095 E, enta Scoop : XTRC 135E, 140E, 150E, 160EN Slam : XTXS 160E, 165 E P Sun : XTCA 170 ET/ ET.1, 180 HE/HE.1 Sun : XTCN 130, 140 E/ Turbo, 143 E Sun : XTCN 150 E, 155 E, 160 E XLence : XTL 190 PE, 210 PE, 212 PET
0402 Atlantic : 404, 405 Bosco : 2419 Domino : 0419 Jolly : 1455 Junior : 0418, 1418 Onyx : 0466, 1466 Viva : 1458, 2458, 7458 Zoom : 1419

SC 33, SC 34A SC 35 SC 35A, 35 AR, 37A /C SC 65 /A, 68A, 75 /A, 76, 79 SC 91, 92 SC 91, 92 SC 400, 410 SC 600, 605, 610 SC 800, 810, 815GR SC 4006 SC T93 SC-N310 SCT 93 Mite Hunter : 1300SC

EC 15P EC : 8300, 8500

BS 13.200 BS 15.100 BS 16.100 TB 13 TB 15 TB 16


Aspira : 1500 Mouse Aspira : 1700 Health Aspira : 1800 Classic Aspira : 1800 King Aspira futur : 2000 Beta : 1200 Compact : 1000, 1200 Delta : 1600 Electronic : 1200 First Class : 1500 Gamma : 1350 Mousy Class : 1300

JC 801 E

AS 1, 2, 3 (magic) B 400 BN 60 Fun, Laser, Rio, Senior 2, Viva S 901 Sx Electronic Sz Automatic T 700, T 1000 Ta Ta Super Taille 9 Tm Lux Tonic Line


ST 1274, 1275, 1276, 1278, 1281, 1284 ST 1283


Tx Ty Tz Electronic 2 Wx Coktail Cyclone : 1000 Cyclone : 2000, 3000 Force : 10 Junior : 5 Junior : / 675 Junior : 1000 Mistral Mistral : 5 Mistral : 2000, 3000, 4000 Silver : 31/5 Sirocco : 5 Stand Supertronic : 2, 3, 4 Supertronic : 5
1004 P 1004 P 1004 P 1004 P 1004 P 1004 P 1004 P 1004 P 5801 P 3502 P P 1802 P 49
Blue Power Comfort Electronic Pico el Premium el Turbo Power
3502 P P P 1802 P 1770 P P P 1802 P 1802 P 1802 P P 1211 P P 1285 P 1802 P 49


VC 130


BSA 1600 BSB 1200 BSC 1200 BSC 1300, BSC 1400 Blue Dancer JC 863


VCS 1800
820.861 TO 7.22 TO 130, 140 TO 170, 180 TO 505, 605 TO 1186, 1900 TO 1863, 1864 TO 2106, 2107 TO 2400.2465 TO 3100.3199 TO 3320 TO 3400 TO 3600 TO 4120 TO 4210, 4212 TO 4425 TO 5037, 5038, 5039 TO 5120 TO 6000, 6002 TO CE 2100, 2300 TOP 520, 530 TR 1.8 TR 100S UC/VC 135, 67 V 5017.4, 5037, 5038 Z 2200, 2230 Z 2260 4X4 : TO 1140.1142 Airmax : TO 6400.6451 Airys : TO 2 Aqualine : TO 810, 813, 815, 820, 823 Aqualine : TO 833, 852, 853, 872, 873 Aventure : TO 465, 466 Aventure : TO 470, 480, 482, 484 Aventure : TO 490 Bolido : 1500.1750 Bolido : TO 4500.4595 Butterfly : TO 6142, 6152, 6162, 6163, 6164 Cadet
C112 M C114 E Jubilee 1200 VB 1100 M VC 1100 M Beetle : 1100 Kever : 1100



SR 1600 SR 2050, 2070


1300 el

Precision TCM TCM TCM TCM TCM TCM TCM TCM TCM TCM 201 506, 211 115

Precision 49 330

B 3106, 3107, 3116 The Mega Boss The Mega Boss Plus XIO


826 SD / SDE
Calypso : TO 6300.6399 Calypso : TO 6510/N, 6520/N, 6521, 6530/N Cameleon : TO 6160, 6165, 6170, 6180, 6190 Campus : TO 4560.4571/N Ciao : TO 1615, 1625, 1635 Complys : TO 200.390 Diamant : 200, 210, 400 Elgance : TO 6600.6630 Elyps : 1110, 1111, 1112A, 1113J, 1114, 1115 Elyps : 1120, 1122A, 1124 Elyps : 1130, 1131, 1132 Essensio : TO 4600.4699 Ex 2000 F1 : TO 2110.2180 Globe Trotteur : TO 1143.1150 Ligne : TO 960T.975 Luxor : TO 486, 490, Turbo Magnum : 4000 B/ N/ O Mega : TO 2330.2335 Mega : TO 2340 B/ N/ R/ T/ V Midyjet, Midyjet Plus Modelys : CA 6200.6230 Modulo : TO 4215, 4216, 4217 Mondo : 1147, 1148, 1149 Multyjet, Multyjet Plus Multyjet, Multyjet Plus : TO 85 Nomad : TO 4411.4415 Peque : TO 1047, 1048, 1049 Perfecto : TO 7010, 7020 Plein Air : 18/A, 20 Plein Air : 200, 250 Pluton : TO 3515, 3525 Quatro : TO 1133.1137 Rolfy : TO 1005, 1055, 1060, 1065, 1067 Rolfy : TO 1070, 1075, 1078, 1079, 1080, 1090 Salsa : TO 1650 Samba Serenys : 6000 B/ BO/ E/ N/ O Serenys : TO 2810.2891 Slalom : TO 2600.2660 Slalom : TO 2700HP.2760HP Smart : TO 1081, 1082 Stratos : TO 467.478 Super Pro : TO 30.50, 55 Turbojet-Plus Twintech : TOT 7740, 7750 Zephir : TO 4621, TO4641



TH-42PWD8EK RT-21FB70V DR-700 A X363DN STR-DB1080 REX T4 DVD-HR757 KD-R303 42PG10 Review FJR1300-2004 Mercury F1 FX100 ZNM11X Almera Handle Adapter KIT Frog Didj Series NV-FJ620A Twister DSC-W220 RSH1deis GA-8IPE1000-G FA168C TM-733A 50PC1RR Multiface 8700F 37PFL9603D 1510XI Indianapolis 7925 SBO-WR37TA MDR-NE2 MS07AH IC7-MAX3 V101 KRC-477RV ES-2044 Kodak M531 Auto-tune EVO Tablet Underdark EL-2196BL 120ED-QD STR-DE898-B WMR968 Carbon Arte SC-PM77MD GVN 53 Dmpbd85 HPI500 PV-GS15 4 5 RP-10 WX-S2200 I-mode 5500I Handheld Palm OS BT620fqst EW-7711UMN VP-D76 Hifax 17 5075E KX-TG8011E SE1402B TX-26LX6F Asus P4BE Powerpod 620 220SW9FB DVP3040K Psma0 CDE-9846R 5045 AHS TX FM 3D View FX-9860G AU VU 2700 Control Unit 305tplus Turbo-9R Fostex 280 Combi Aficio 3045 ESD-9000 HD400LD Activ Life Infiniti QX4 Yamaha FS1R MP3-3130R UBT780 SGH-I750 14 0 L1950H-SN SA-EX320 PDP-R06FE ES-2058 RM-V202 VP-D73 MHC550


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