Blair M L, Chen Y H, Hisa H
Am J Physiol. 1986 Dec;251(6 Pt 1):E695-702. doi: 10.1152/ajpendo.1986.251.6.E695.
Experiments were performed in conscious trained dogs to determine whether renal alpha-adrenergic receptors mediate stimulation or inhibition of renin release. All dogs were uninephrectomized and surgically prepared with chronically indwelling catheters in the aorta, vena cava, and remaining renal artery at least 8 days before experiment. Direct renal artery (ia) infusion of the alpha-adrenoceptor agonist phenylephrine, 0.25 or 0.50 microgram X kg-1 X min-1 for 30 min, increased plasma renin activity (PRA) to 145 +/- 13 and 212 +/- 28% of control, respectively, within 5 min of drug infusion (P less than 0.01) in conscious sodium-replete dogs. In contrast, intravenous phenylephrine infusion decreased PRA by 50% (P less than 0.001). The increase in PRA observed during ia phenylephrine infusion was prevented by renal alpha-adrenoceptor blockade with phenoxybenzamine but not by beta-adrenoceptor blockade with propranolol. Methoxamine, another alpha-adrenoceptor agonist, also increased PRA when infused ia in both sodium-replete dogs and in dogs maintained on a low-sodium diet. In dogs with renal arterial electromagnetic flowprobes, ia phenylephrine infusion increased PRA without decreasing total renal blood flow. In summary, stimulation of renal alpha-adrenoceptors increases PRA in conscious dogs. This stimulation can occur in the absence of significant changes in total renal blood flow.
在清醒的经训练犬身上进行实验,以确定肾α-肾上腺素能受体是介导肾素释放的刺激还是抑制。所有犬均行单侧肾切除术,并在实验前至少8天通过手术将慢性留置导管置于主动脉、腔静脉和剩余肾动脉内。在清醒的钠充足犬中,经肾动脉(ia)直接输注α-肾上腺素能受体激动剂去氧肾上腺素,剂量为0.25或0.50微克·千克⁻¹·分钟⁻¹,持续30分钟,在药物输注后5分钟内,血浆肾素活性(PRA)分别升高至对照值的145±13%和212±28%(P<0.01)。相比之下,静脉输注去氧肾上腺素使PRA降低了50%(P<0.001)。经肾动脉输注去氧肾上腺素期间观察到的PRA升高,可被用酚苄明进行的肾α-肾上腺素能受体阻断所阻止,但不能被用普萘洛尔进行的β-肾上腺素能受体阻断所阻止。另一种α-肾上腺素能受体激动剂甲氧明,在钠充足犬和低钠饮食犬经肾动脉输注时也能增加PRA。在安装了肾动脉电磁血流探头的犬中,经肾动脉输注去氧肾上腺素增加PRA但不降低肾总血流量。总之,刺激肾α-肾上腺素能受体可增加清醒犬的PRA。这种刺激可在肾总血流量无显著变化的情况下发生。