Acetylcholine-induced vasodilation without natriuresis during control of interstitial pressure.
Acetylcholine-induced vasodilation without natriuresis during control of interstitial pressure.
复制标题
在控制间质压力期间乙酰胆碱诱导的血管舒张而无尿钠排泄。
DOI：
10.1152/ajprenal.1982.243.4.f325
复制
发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Knox,FG
中科院分区：
文献类型：
--
作者：
Hartupee,DA;BurnettJr,JC;Mertz,JI;Knox,FG
Increased renal blood flow and increased renal interstitial pressure have been proposed as mechanisms for the natriuresis caused by vasodilation with acetylcholine. We tested the hypothesis that the natriuresis due to acetylcholine is associated with the increase in interstitial pressure rather than with the increase in blood flow. Experiments were performed in decapsulated kidneys that, along with partial aortic clamping, allowed dissociation of the increases in renal interstitial pressure and blood flow. At the beginning of intrarenal acetylcholine infusion (2 micrograms . kg-1 . min-1), the aorta was clamped so that a vasodilation occurred without an increase in interstitial pressure. A response to acetylcholine was also obtained when interstitial pressure was allowed to increase. During this response, renal blood flow, interstitial pressure, and fractional sodium excretion increased. During control of interstitial pressure, renal blood flow increased, but fractional sodium excretion did not change. Thus, when interstitial pressure was controlled, the acetylcholine-induced vasodilation did not result in an increase in fractional sodium excretion. These results demonstrate that an increase in renal interstitial pressure is required for the natriuresis associated with acetylcholine-induced vasodilation.
