Role of nitric oxide in modulating the long-term renal and hypertensive actions of norepinephrine.

Role of nitric oxide in modulating the long-term renal and hypertensive actions of norepinephrine.
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一氧化氮在调节去甲肾上腺素的长期肾脏和高血压作用中的作用。

DOI:
10.1161/01.hyp.29.1.205
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发表时间:
1997
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Kassab,S
Kassab,S
中科院分区:
--
文献类型:
--
作者:
Granger,J;Schnackenberg,C;Novak,J;Tucker,B;Miller,T;Morgan,S;Kassab,S

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我们以前曾报道,一氧化氮(NO)在保护肾血管免受急性去甲肾上腺素诱导的血管收缩中起着重要作用。本研究的目的是确定NO和去甲肾上腺素之间的这种相互作用在长期控制肾血流动力学和动脉压的重要性。为了实现这一目标,我们在清醒的慢性仪器对照犬和用合成抑制剂L-NAME(3 μg·kg−1·min− 1肾内)预处理的犬中检查了肾内输注去甲肾上腺素(NE)(0.1 μg·kg − 1·min −1)7天的效果。两组犬在整个研究过程中还接受了卡托普利(15 μg·kg-1·min-1)和血管紧张素II静脉给药,以阻断肾素-血管紧张素系统。在对照犬(n=6)中,肾内输注NE使肾血浆流量降低9%(134±10至122±14 mL/min),肾小球滤过率降低16%(49±4至41±5 mL/min),而对平均动脉压无影响(100±3至98±4 mm Hg)。与此相反,在肾内注射L-NAME的狗(n=9)中,NE使肾血浆流量降低37%(129±8至81±16 mL/min),肾小球滤过率降低32%(47±3至32±5 mL/min),而平均动脉压从104±5升高至113±6 mm Hg。本研究结果表明,NO在调节NE对肾功能和动脉压的长期作用中起重要作用。
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−1intrarenally). 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.