Why the study?
Does chronic intrarenal NO synthesis blockade modulate the chronic renal and arterial pressure responses to angiotensin II in dogs?
Does chronic intrarenal NO synthesis blockade modulate the chronic renal and arterial pressure responses to angiotensin II in dogs?
Chronic inhibition of NO synthesis within the kidney attenuates the long-term renal and arterial pressure responses to angiotensin II in dogs.
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Chronic intrarenal NO inhibition blunts AII responses in dogs; leaves open any role in human hypertension.
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(omega)-nitro-L-arginine methyl ester (3 micrograms/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 by AII in dogs.
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Christine G. Schnackenberg (1997) studied this question.
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