Role of Nitric Oxide in Modulating the Long-term Renal and Hypertensive Actions of Norepinephrine

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Abstract
We have previously reported that nitric oxide (NO) plays an important role in protecting the renal vasculature from acute norepinephrine-induced vasoconstriction. The purpose of this study was to determine the importance of this interaction between NO and norepinephrine in long-term control of renal hemodynamics and arterial pressure. To achieve this goal, we examined the effects of an intrarenal infusion of norepinephrine (NE) (0.1 μg·kg −1 ·min −1 ) for 7 days in conscious, chronically instrumented control dogs and in dogs pretreated with a synthesis inhibitor, L-NAME (3 μg·kg −1 ·min −1 intrarenally). Both groups of dogs also received captopril (15 μg·kg −1 ·min −1 ) plus angiotensin II intravenously to clamp the renin-angiotensin system throughout the protocol. In control dogs (n=6), intrarenal infusion of NE decreased renal plasma flow by 9% (134±10 to 122±14 mL/min) and glomerular filtration rate by 16% (49±4 to 41±5 mL/min) while having no effect on mean arterial pressure (100±3 to 98±4 mm Hg). In marked contrast, in dogs pretreated with intrarenal L-NAME (n=9), NE decreased renal plasma flow by 37% (129±8 to 81±16 mL/min) and glomerular filtration rate by 32% (47±3 to 32±5 mL/min) while increasing mean arterial pressure from 104±5 to 113±6 mm Hg. The results of this study demonstrate that NO plays an important role in modulating the long-term actions of NE on renal function and arterial pressure.