Abstract

Normal renal function requires stable renal blood flow. It is achieved by autoregulation. Nitric oxide contributes to the regulation of multiple pathways that are relevant to myogenic autoregulation. We examined the signal transduction mechanism of nitric oxide on myogenic autoregulation in the present thesis. Because some paracrine factors contribute to the renal autoregulation, we first isolate the effects of nitric oxide from other paracrine factors. The pressor and renal vasoconstrictor responses to nitric oxide synthase inhibition are independent of angiotensin II. There is an interaction between nitric oxide and endothelin, mediated by endothelin B receptors, that affects renal blood flow and renal autoregulation. Y-27632, Rho-kinase inhibitor reverses completely the enhanced myogenic autoregulation by L-NAME, and L-NAME does not affect the myogenic autoregulation pre-treated by Y27632. In conclusion, the effect of Rho-kinase with consequent inhibition of myosin light chain phosphatase may be an essential component of the modulation of myogenic autoregulation by nitric oxide. Therefore, the signal transudation of nitric oxide on renal autoregulation passes through Rho-kinase pathway.

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