Hartupee D A, Burnett J C, Mertz J I, Knox F G
Am J Physiol. 1982 Oct;243(4):F325-9. doi: 10.1152/ajprenal.1982.243.4.F325.
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.
肾血流量增加和肾间质压力升高被认为是乙酰胆碱介导的血管舒张所致利钠作用的机制。我们验证了这样一个假设，即乙酰胆碱引起的利钠作用与间质压力升高有关，而非与血流量增加有关。实验在去包膜的肾脏上进行，该实验连同部分主动脉夹闭，能够区分肾间质压力升高和血流量增加。在肾内输注乙酰胆碱（2微克·千克⁻¹·分钟⁻¹）开始时，夹闭主动脉，使得血管舒张时间质压力不升高。当允许间质压力升高时，也能获得对乙酰胆碱的反应。在此反应过程中，肾血流量、间质压力和钠排泄分数增加。在控制间质压力期间，肾血流量增加，但钠排泄分数没有变化。因此，当间质压力得到控制时，乙酰胆碱诱导的血管舒张并未导致钠排泄分数增加。这些结果表明，乙酰胆碱诱导的血管舒张相关的利钠作用需要肾间质压力升高。
