Rho kinase regulates renal blood flow by modulating eNOS activity in ischemia-reperfusion of the rat kidney
| Autor: | Iolente J M Korstjens, Pieter Sipkema, Amanda M. G. Versteilen, René J. P. Musters, A. B. Johan Groeneveld |
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| Rok vydání: | 2006 |
| Předmět: |
Male
medicine.medical_specialty Nitric Oxide Synthase Type III Physiology Ischemia Rat kidney Vasodilation Protein Serine-Threonine Kinases Kidney Renal Circulation Norepinephrine Renal Artery Enos Internal medicine medicine Animals Rats Wistar Rho-associated protein kinase rho-Associated Kinases biology business.industry Microfilament Proteins Hemodynamics Intracellular Signaling Peptides and Proteins Vasodilator-stimulated phosphoprotein Blood flow Phosphoproteins medicine.disease biology.organism_classification Acetylcholine Rats NG-Nitroarginine Methyl Ester Endocrinology Reperfusion Injury Renal blood flow business Cell Adhesion Molecules |
| Zdroj: | American Journal of Physiology-Renal Physiology. 291:F606-F611 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.00434.2005 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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