Effect of Rho Kinase Inhibitor on the Production of Nitric Oxide in Trabecular Meshwork Cells

2016 ◽  
Vol 57 (4) ◽  
pp. 650 ◽  
Author(s):  
Jae Woo Kim ◽  
Keun Hae Kim ◽  
Seok Jin Hwang
Keyword(s):  
Nitric Oxide ◽  
Trabecular Meshwork ◽  
Kinase Inhibitor ◽  
Rho Kinase ◽  
Trabecular Meshwork Cells ◽  
Rho Kinase Inhibitor

Rho kinase regulates renal blood flow by modulating eNOS activity in ischemia-reperfusion of the rat kidney

2006 ◽  
Vol 291 (3) ◽  
pp. F606-F611 ◽  
Author(s):  
Amanda M. G. Versteilen ◽  
Iolente J. M. Korstjens ◽  
René J. P. Musters ◽  
A. B. Johan Groeneveld ◽  
Pieter Sipkema
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Kinase Inhibitor ◽  
Ex Vivo ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Rho Kinase ◽  
Rho Kinase Inhibitor

Renal ischemia-reperfusion (I/R) results in vascular dysfunction characterized by a reduced endothelium-dependent vasodilatation and subsequently impaired blood flow. In this study, we investigated the role of Rho kinase in endothelial nitric oxide synthase (eNOS)-mediated regulation of renal blood flow and vasomotor tone in renal I/R. Male Wistar rats were subjected to 60-min bilateral clamping of the renal arteries or sham procedure. One hour before the clamping, the Rho kinase inhibitor Y27632 (1 mg/kg) was intravenously infused. After I/R, renal blood flow was measured using fluorescent microspheres. I/R resulted in a 62% decrease in renal blood flow. In contrast, the blood flow decrease in the group treated with the Rho kinase inhibitor (YI/R) was prevented. Endothelium-dependent vasodilatation of renal arcuate arteries to ACh was measured ex vivo in a pressure myograph. These experiments demonstrated that the in vivo treatment with the Rho kinase inhibitor prevented the decrease in the nitric oxide (NO)-mediated vasodilator response. In addition, after I/R renal interlobar arteries showed a decrease in phosphorylated eNOS and vasodilator-stimulated phosphoprotein, a marker for bioactive NO, which was attenuated by in vivo Rho kinase inhibition. These findings indicate that in vivo inhibition of Rho kinase in renal I/R preserves renal blood flow by improving eNOS function.

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