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肾上腺素诱导的肾素分泌并非由心脏肾上腺素能受体启动。

Epinephrine-induced renin secretion is not initiated by cardiac adrenoceptors.

作者信息

Johnson M D, Whitener C J, Sears T S

机构信息

Department of Physiology, West Virginia University, Morgantown 26506.

出版信息

Am J Physiol. 1988 Mar;254(3 Pt 1):E265-71. doi: 10.1152/ajpendo.1988.254.3.E265.

DOI:10.1152/ajpendo.1988.254.3.E265
PMID:3279810
Abstract

Experiments were designed to test the hypothesis that epinephrine may act directly on cardiac or pulmonary adrenoceptors to alter the release of a humoral substance that in turn influences renin secretion. Accordingly, anesthetized dogs were prepared with catheters for infusion of epinephrine at three sites: 1) into the aorta just distal to the left subclavian artery, 2) into the left ventricle, and 3) near the right atrium. Left renal renin secretion rates were determined before, during, and after 30-min infusions of epinephrine at each site in each animal; the order of the infusions was randomized. At epinephrine infusion rates of 15 and 75 ng.kg-1.min-1, epinephrine-induced changes in renin secretion rates were dose dependent but were independent of the site of infusion. These data do not support the hypotheses that either pulmonary or cardiac adrenoceptors are involved in the initiation of epinephrine-induced renin secretion. In additional experiments, an isolated canine heart was perfused with femoral arterial blood from an experimental dog, and the coronary venous effluent was returned to the experimental dog via the femoral vein. Intravenous epinephrine infusion at 50 ng.kg-1.min-1 increased plasma renin activity nearly 1.5-fold. In contrast, plasma renin activity did not increase during infusion of epinephrine at 5 ng.kg-1.min-1 directly into the coronary perfusate of the isolated heart. Coronary perfusate epinephrine concentration was 699 +/- 71 pg/ml (mean +/- SE) during intravenous infusion and was 851 +/- 121 pg/ml during direct infusion of epinephrine into the coronary perfusate. We conclude that cardiac adrenoceptors do not participate in the initiation of epinephrine-induced renin secretion.

摘要

实验旨在检验肾上腺素可能直接作用于心脏或肺的肾上腺素能受体,从而改变一种体液物质的释放,进而影响肾素分泌这一假说。因此,给麻醉的狗插入导管,以便在三个部位输注肾上腺素:1)在左锁骨下动脉远端的主动脉内;2)在左心室内;3)在右心房附近。在每只动物的每个部位输注肾上腺素30分钟之前、期间和之后,测定左肾肾素分泌率;输注顺序是随机的。在肾上腺素输注速率为15和75 ng.kg-1.min-1时,肾上腺素引起的肾素分泌率变化呈剂量依赖性,但与输注部位无关。这些数据不支持肺或心脏肾上腺素能受体参与肾上腺素诱导的肾素分泌起始过程的假说。在另外的实验中,用来自实验狗的股动脉血灌注离体犬心脏,冠状动脉静脉流出液通过股静脉返回实验狗体内。以50 ng.kg-1.min-1的速率静脉输注肾上腺素,使血浆肾素活性增加近1.5倍。相比之下,以5 ng.kg-1.min-1的速率将肾上腺素直接输注到离体心脏的冠状动脉灌注液中时,血浆肾素活性并未增加。静脉输注期间冠状动脉灌注液中的肾上腺素浓度为699 +/- 71 pg/ml(平均值 +/- 标准误),将肾上腺素直接输注到冠状动脉灌注液中时为851 +/- 121 pg/ml。我们得出结论,心脏肾上腺素能受体不参与肾上腺素诱导的肾素分泌起始过程。

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