NITRIC-OXIDE ATTENUATES THE RENAL HEMODYNAMIC-RESPONSES TO INCREASED PERIPHERAL AND RENAL SYMPATHETIC-NERVE ACTIVITY

The role of nitric oxide (NO) in renal function was evaluated under co nditions of elevated peripheral and renal sympathetic nerve activity ( RSNA), achieved by bilateral carotid occlusion (GO) in anesthetized do gs. Renal function was monitored during CO with the NO system intact a nd with it blocked by the administration of L-NAME, With NO intact, CO increased arterial pressure and heart rate. With renal perfusion pres sure held constant, CO also significantly decreased renal blood flow ( RBF) acid glomerular filtration rate (GFR) by 46% and 43%, respectivel y. CO, after L-NAME administration, resulted in a significantly exagge rated renal vasoconstriction. RBF and GFR decreased by 82% and 80%, re spectively. Changes in water and sodium excretion were not different b etween the NO-intact and NO-blocked states during CO. These studies we re also performed with the converting enzyme inhibitor, Captopril. The exaggerated renal hemodynamic responses to CO with NO synthesis inhib ition were identical with or without Captopril. These findings indicat e that under conditions of elevated peripheral and RSNA, NO plays an i mportant role in modulating renal hemodynamics, but not sodium excreti on. This effect does not appear to involve angiotensin II.