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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Gastrointestinal and Liver Physiology|
|State||Published - 1988|
All Science Journal Classification (ASJC) codes
- Physiology (medical)