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 conditions of elevated peripheral and renal sympathetic nerve activity (RSNA), achieved by bilateral carotid occlusion (CO) in anesthetized dogs. Renal function was monitored during CO with the NO system intact and with it blocked by the administration of L-NAME. With NO intact, CO increased arterial pressure and heart rate. With renal perfusion pressure held constant, CO also significantly decreased renal blood flow (RBF) and glomerular filtration rate (GFR) by 46% and 43%, respectively. CO, after L-NAME administration, resulted in a significantly exaggerated renal vasoconstriction. RBF and GFR decreased by 82% and 80%, respectively. Changes in water and sodium excretion were not different between the NO-intact and NO-blocked states during CO. These studies were also performed with the converting enzyme inhibitor, Captopril. The exaggerated renal hemodynamic responses to CO with NO synthesis inhibition were identical with or without Captopril. These findings indicate that under conditions of elevated peripheral and RSNA, NO plays an important role in modulating renal hemodynamics, but not sodium excretion. This effect does not appear to involve angiotensin II.