Abstract
The purpose of this study was to determine long-term role of nitric oxide in modulating the chronic renal and arterial pressure responses to angiotensin II (AII). In normal dogs, intrarenal AII infusion (1.0 ng/kg/min) decreased renal plasma flow (RPF) by 31% and glomerular filtration rate (GFR) by 17% and increased mean arterial pressure (MAP) by 22%. In dogs with chronic intrarenal NO synthesis blockade with N ω -nitro- l-arginine methyl ester (3 μg/kg/min), AII decreased RPF by 25% and GFR by 19%, and increased MAP by 7%. These data indicate that chronic inhibition of NO synthesis within the kidney attenuated the long-term renal and arterial pressure responses to AII in dogs.
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