Blair M L
Am J Physiol. 1983 Jan;244(1):E37-44. doi: 10.1152/ajpendo.1983.244.1.E37.
This study was designed to determine whether stimulation of intrarenal alpha-adrenoceptors can increase renin secretion rate (RSR) in the absence of increased renal vascular resistance and to identify the accompanying changes in renal function. Experiments were performed in pentobarbital-anesthetized dogs in which renal perfusion pressure was maintained at approximately 90 mmHg and the infused kidney was acutely denervated. Renal artery infusion of the alpha-adrenoceptor agonist methoxamine (0.5 microgram X kg-1 X min-1 for 30 min) increased RSR from 160 +/- 95 to 1,376 +/- 385 ng ANG I/min (P = 0.01) but did not decrease renal blood flow (RBF); the same dose infused intravenously had no effect on RSR or RBF. Intra-arterial phenylephrine infusion (0.5 microgram X kg-1 X min-1 for 9 min) increased RSR by 500 +/- 157 ng ANG I/min (P less than 0.01) and decreased both inulin clearance (Cin) and urinary sodium excretion (UNaV) by 25% but did not affect RBF. At a lower concentration of phenylephrine (0.2 microgram X kg-1 X min-1 for 9 min), RSR increased by 318 +/- 103 ng ANG I/min (P less than 0.01) and RBF, Cin, and UNaV did not change. The increase in RSR was completely blocked by prazosin but was unaffected by propranolol. In summary, renin secretion can be stimulated by activation of intrarenal alpha-adrenoceptors even in the absence of increased renal vascular resistance.
本研究旨在确定在肾血管阻力未增加的情况下,刺激肾内α-肾上腺素能受体是否能提高肾素分泌率(RSR),并确定伴随的肾功能变化。实验在戊巴比妥麻醉的犬身上进行,维持肾灌注压在约90 mmHg,并对灌注的肾脏进行急性去神经支配。肾动脉输注α-肾上腺素能受体激动剂甲氧明(0.5微克/千克/分钟,持续30分钟)使RSR从160±95增加到1376±385纳克血管紧张素I/分钟(P = 0.01),但未降低肾血流量(RBF);相同剂量静脉输注对RSR或RBF无影响。动脉内输注去氧肾上腺素(0.5微克/千克/分钟,持续9分钟)使RSR增加500±157纳克血管紧张素I/分钟(P<0.01),使菊粉清除率(Cin)和尿钠排泄(UNaV)均降低25%,但不影响RBF。在较低浓度的去氧肾上腺素(0.2微克/千克/分钟,持续9分钟)时,RSR增加318±103纳克血管紧张素I/分钟(P<0.01),而RBF、Cin和UNaV未改变。RSR的增加被哌唑嗪完全阻断,但不受普萘洛尔影响。总之,即使在肾血管阻力未增加的情况下,肾内α-肾上腺素能受体的激活也能刺激肾素分泌。