scholarly journals Differential effects of Rho-kinase inhibitor and angiotensin II type-1 receptor antagonist on the vascular function in hypertensive rats induced by chronic l-NAME treatment

2012 ◽  
Vol 2 (5) ◽  
pp. 450-458 ◽  
Author(s):  
Bainian Chen ◽  
Lili Shi ◽  
Xiaoyan Yu ◽  
Jialin Sun ◽  
Hengai Zhang ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Receptor Antagonist ◽  
Vascular Function ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Hypertensive Rats ◽  
Differential Effects ◽  
Rho Kinase Inhibitor

Fasudil, a Rho-kinase inhibitor, reverses L-NAME exacerbated severe nephrosclerosis in spontaneously hypertensive rats

2008 ◽  
Vol 26 (9) ◽  
pp. 1837-1848 ◽  
Author(s):  
Shogo Koshikawa ◽  
Toshio Nishikimi ◽  
Chikako Inaba ◽  
Kazumi Akimoto ◽  
Hiroaki Matsuoka
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Rho Kinase Inhibitor

scholarly journals Sex differences in the enhanced responsiveness to acute angiotensin II in growth-restricted rats: role of fasudil, a Rho kinase inhibitor

2013 ◽  
Vol 304 (7) ◽  
pp. F900-F907 ◽  
Author(s):  
Norma B. Ojeda ◽  
Thomas P. Royals ◽  
Barbara T. Alexander
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Ang Ii ◽  
Intact Male ◽  
Rho Kinase Inhibitor

This study tested the hypothesis that Rho kinase contributes to the enhanced pressor response to acute angiotensin II in intact male growth-restricted and gonadectomized female growth-restricted rats. Mean arterial pressure (MAP) and renal function were determined in conscious animals pretreated with enalapril (250 mg/l in drinking water) for 1 wk to block the endogenous renin-angiotensin system and normalize blood pressure (baseline). Blood pressure and renal hemodynamics did not differ at baseline. Acute Ang II (100 ng·kg−1·min−1) induced a greater increase in MAP and renal vascular resistance and enhanced reduction in glomerular filtration rate in intact male growth-restricted rats compared with intact male controls ( P < 0.05). Cotreatment with the Rho kinase inhibitor fasudil (33 μg·kg−1·min−1) significantly attenuated these hemodynamic changes ( P < 0.05), but it did not abolish the differential increase in blood pressure above baseline, suggesting that the impact of intrauterine growth restriction on blood pressure in intact male growth-restricted rats is independent of Rho kinase. Gonadectomy in conjunction with fasudil returned blood pressure back to baseline in male growth-restricted rats, and yet glomerular filtration rate remained significantly reduced ( P < 0.05). Thus, these data suggest a role for enhanced renal sensitivity to acute Ang II in the developmental programming of hypertension in male growth-restricted rats. However, inhibition of Rho kinase had no effect on the basal or enhanced increase in blood pressure induced by acute Ang II in the gonadectomized female growth-restricted rat. Therefore, these studies suggest that Rho kinase inhibition exerts a sex-specific effect on blood pressure sensitivity to acute Ang II in growth-restricted rats.

Proinsulin C-peptide constricts glomerular afferent arterioles in diabetic mice. A potential renoprotective mechanism

2008 ◽  
Vol 294 (3) ◽  
pp. R836-R841 ◽  
Author(s):  
Lina Nordquist ◽  
En Yin Lai ◽  
Mats Sjöquist ◽  
Andreas Patzak ◽  
A. Erik G. Persson
Keyword(s):  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Diabetic Animal ◽  
Diabetic Mice ◽  
C Peptide ◽  
Control Value ◽  
Rho Kinase Inhibitor ◽  
Afferent Arterioles ◽  
Design And Methods

Objective: an increased glomerular filtration rate (GFR) has been postulated as a potential mechanism involved in the progression of diabetic nephropathy. Studies suggest that C-peptide exerts a renoprotective effect on diabetes. The peptide decreases hyperfiltration in patients with type 1 diabetes, as well as in diabetic animal models. In this study, we investigated whether C-peptide causes a change in arteriolar diameter. Research Design and Methods: C57-Bl mice were made diabetic by means of a single intravenous injection of alloxan 2 wk prior to the experiment. Age-matched normoglycemic mice served as controls. Afferent arterioles, intact with the glomeruli, were dissected and microperfused. The effect of luminal application of C-peptide, compared with scrambled C-peptide or vehicle, was investigated. The effect of the Rho-kinase inhibitor Y-27632 was also investigated. Results: C-peptide constricted afferent arterioles in diabetic mice by −27% compared with the control value. Normoglycemic arterioles administered C-peptide displayed a delayed and minute response (−4%). Scrambled C-peptide or vehicle administration, whether administered to hyperglycemic or normoglycemic mice, did not induce any effect. Addition of Y-27632 abolished the effect of C-peptide. Conclusion: C-peptide induces constriction of afferent arterioles in diabetic mice. This can reduce enhanced GFR and may be one of the mechanisms in the renoprotective action of C-peptide in diabetes.

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