Takahashi K, Hisa H, Satoh S
J Cardiovasc Pharmacol. 1984 Mar-Apr;6(2):251-5. doi: 10.1097/00005344-198403000-00007.
We examined the relationship between prostaglandin (PG) production and renin release induced by a nonvasoconstrictor dose of an alpha-agonist, phenylephrine, in anesthetized dogs. Intrarenal infusion of phenylephrine (1 microgram/min) did not affect systemic blood pressure or renal blood flow, but increased the renin secretion rate about twofold. The effect of phenylephrine on renin release was abolished by the intrarenal infusion of the alpha-antagonist phentolamine (50 micrograms/min), but was not affected by the intravenous administration of the PG synthetase inhibitor indomethacin (5 mg/kg). Urine flow and urinary sodium excretion rate were not altered by phenylephrine. These results suggest that a nonvascular and nontubular alpha-adrenoceptor mechanism, which is independent of the renal PG system, may be involved in renin release.
我们研究了在麻醉犬中,非血管收缩剂量的α-激动剂去氧肾上腺素诱导的前列腺素(PG)生成与肾素释放之间的关系。肾内输注去氧肾上腺素(1微克/分钟)不影响全身血压或肾血流量,但使肾素分泌率增加约两倍。肾内输注α-拮抗剂酚妥拉明(50微克/分钟)可消除去氧肾上腺素对肾素释放的作用,但静脉注射PG合成酶抑制剂吲哚美辛(5毫克/千克)对其无影响。去氧肾上腺素未改变尿流量和尿钠排泄率。这些结果表明,一种独立于肾PG系统的非血管和非肾小管α-肾上腺素能受体机制可能参与肾素释放。