Abstract

Previous experiments have demonstrated that increments of circulating epinephrine concentration within the physiological range elevate PRA and that this effect apparently is mediated by extrarenal beta-adrenoceptors. The present experiments were designed to test the possibility that the receptors mediating the PRA response to epinephrine are located in the splanchnic region. Accordingly, adult dogs were anesthetized, and catheters were placed for recording blood pressure, withdrawal of blood samples, and collection of urine. Infusion catheters were placed in a femoral vein and in the celiac and superior mesenteric arteries. After a control period, epinephrine was infused for 45 min at a total rate of 25 ng kg-1 min-1 either iv or directly into the celiac and superior mesenteric arteries (12.5 ng kg-1 min-1 into each artery simultaneously). Renal perfusion pressure was kept at the control level during the infusion period by means of an adjustable suprarenal aortic clamp. PRA rose from a mean control plus recovery value of 4.5 +/- 0.9 ng ml-1 h-1 to 8.7 +/- 0.7 ng ml-1 h-1 during iv epinephrine infusion. In contrast, PRA remained unchanged (3.9 +/- 0.8 vs. 4.3 +/- 1.1 ng ml-1 h-1) in response to infusion of epinephrine directly into the celiac and superior mesenteric arteries. The data indicate that the receptors mediating epinephrine-induced increases in PRA are not located in organs perfused by the celiac and superior mesenteric arteries.

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