Plasma epinephrine and control of plasma renin activity: possible extrarenal mechanisms.
Previous work from our laboratory has shown that physiological increments of circulating epinephrine concentration increase plasma renin activity (PRA) by an extrarenal beta-receptor mechanism. In the present experiments, epinephrine was infused intravenously at 125 ng.kg-1.min-1 for 45 min in trained, conscious dogs. PRA rose 3 to 5-fold, as previously described, and was accompanied by a transient decline of mean arterial pressure, decreased plasma potassium concentration, and increased hematocrit. Prior splenectomy to maintain hematocrit constant did not attenuate the PRA response to epinephrine. The kidneys of 4 dogs were denervated and constrictor cuff was placed around the renal artery. Renal denervation did not alter the PRA response to intravenous epinephrine infusion. A transient decline in renal perfusion pressure produced by cuff constriction only transiently increase PRA. Neither maintenance of a constant plasma potassium concentration nor oral administration of indomethacin altered the PRA response to epinephrine. We conclude that intravenous epinephrine increases PRA by a mechanism independent of the renal nerves, changes in renal perfusion pressure, hematocrit, plasma potassium concentration, and plasma prostaglandins.
D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003714:Denervation; D004285:Dogs; D004837:Epinephrine / Q000097:blood*; D005260:Female; D006400:Hematocrit; D007213:Indomethacin / Q000494:pharmacology; D007668:Kidney / Q000294:innervation*; D008297:Male; D011188:Potassium / Q000097:blood; D011453:Prostaglandins / Q000097:blood; D012083:Renin / Q000097:blood*
D011453:Prostaglandins; D012083:Renin; D011188:Potassium; D007213:Indomethacin; D004837:Epinephrine