Johnson M D, Fahri E R, Troen B R, Barger A C
Am J Physiol. 1979 Jun;236(6):H854-9. doi: 10.1152/ajpheart.1979.236.6.H854.
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.
我们实验室之前的研究表明，循环中肾上腺素浓度的生理性升高通过肾外β受体机制增加血浆肾素活性（PRA）。在本实验中，对训练有素的清醒犬静脉输注肾上腺素，剂量为125 ng·kg-1·min-1，持续45分钟。如前所述，PRA升高了3至5倍，同时伴有平均动脉压短暂下降、血浆钾浓度降低和血细胞比容升高。事先进行脾切除术以维持血细胞比容恒定，并未减弱PRA对肾上腺素的反应。对4只犬进行肾去神经支配，并在肾动脉周围放置收缩套。肾去神经支配并未改变PRA对静脉输注肾上腺素的反应。由套扎引起的肾灌注压短暂下降仅使PRA短暂升高。维持恒定的血浆钾浓度或口服吲哚美辛均未改变PRA对肾上腺素的反应。我们得出结论，静脉注射肾上腺素通过一种独立于肾神经、肾灌注压变化、血细胞比容、血浆钾浓度和血浆前列腺素的机制增加PRA。
