ANGIOTENSIN-II-INDUCED RENAL RESPONSES IN ANESTHETIZED RABBITS - EFFECTS OF N(OMEGA-)NITRO-L-ARGININE METHYL-ESTER AND LOSARTAN

Intrarenal arterial infusion of angiotensin II (4 ng/kg/min) reduced r enal blood flow, glomerular filtration rate and urinary Na+ excretion (UNaV) without affecting fractional Na+ excretion (FENa) in anesthetiz ed rabbits. Losartan (10 mu g/kg/min) abolished these angiotensin II-i nduced renal responses. The renal blood flow, glomerular filtration ra te and UNaV responses were potentiated during intrarenal arterial infu sion of N-omega-nitro-L-arginine methyl ester (L-NAME, 10 mu g/kg/min) . A high dose of L-NAME (50 mu g/kg/min) also potentiated the renal bl ood flow and UNaV responses but not the glomerular filtration rate res ponse. Angiotensin II reduced FENa during L-NAME infusion at either do se. In L-NAME-pretreated rabbits, losartan abolished the angiotensin i i-induced renal blood flow and glomerular filtration rate responses, b ut the reduction in FENa still remained. The present study suggests th at in the rabbit kidney (1) nitric oxide attenuates the angiotensin II -induced (angiotensin AT1 receptor-mediated) vasoconstriction and (2) angiotensin II can evoke losartan-resistant tubular Na+ reabsorption, but the tubular action is concealed by nitric oxide.