Holdaas H, DiBona G F, Kiil F
Am J Physiol. 1981 Aug;241(2):F156-61. doi: 10.1152/ajprenal.1981.241.2.F156.
The mechanism whereby renal nerves influence the renin-release response to aortic constriction was examined in a nonfiltering ureter-occluded kidney preparation in anesthetized dogs. The kidney was rendered nonfiltering by a combination of mannitol infusion and ureteral occlusion. Suprarenal aortic constriction reduced renal perfusion pressure to 61 +/- 7 mmHg and increased renin release from 16.7 +/- 4.1 to 26.1 +/- 6.0 U/min. At normal renal perfusion pressure, low-frequency renal nerve stimulation (0.25 Hz) increased renin release by 11.6 +/- 4.2 to 25.1 +/- 7.6 U/min. The effect of combined low-level renal nerve stimulation and aortic constriction on renin release was additive; renin release increased by 24.6 +/- 6.5 to 39.5 +/- 7.3 U/min. Propranolol or metoprolol, administered intrarenally at 2 microgram . min-1 . kg-1, abolished the renin-release response to low-level renal nerve stimulation at normal renal perfusion pressure. These data provide evidence that low-frequency renal nerve stimulation influences the renin-release response to reduction in renal perfusion pressure in a nonfiltering ureter-occluded kidney with an inoperative macula densa receptor mechanism. The neural effect on renin release at normal renal perfusion pressure is mediated via beta 1-adrenoceptors probably located on the juxtaglomerular granular cells.
在麻醉犬的无滤过功能的输尿管阻塞肾制备模型中，研究了肾神经影响肾素释放对主动脉缩窄反应的机制。通过输注甘露醇和输尿管阻塞相结合的方法使肾脏失去滤过功能。肾上腺上方的主动脉缩窄使肾灌注压降至61±7 mmHg，并使肾素释放从16.7±4.1 U/min增加到26.1±6.0 U/min。在正常肾灌注压下，低频肾神经刺激（0.25 Hz）使肾素释放从11.6±4.2 U/min增加到25.1±7.6 U/min。低水平肾神经刺激与主动脉缩窄联合作用对肾素释放的影响是相加的；肾素释放增加到24.6±6.5 U/min至39.5±7.3 U/min。以2 μg·min-1·kg-1的剂量肾内给予普萘洛尔或美托洛尔，可消除在正常肾灌注压下低水平肾神经刺激引起的肾素释放反应。这些数据表明，在无滤过功能的输尿管阻塞肾且致密斑受体机制不起作用的情况下，低频肾神经刺激影响肾素释放对肾灌注压降低的反应。在正常肾灌注压下，神经对肾素释放的作用可能通过位于肾小球旁颗粒细胞上的β1-肾上腺素能受体介导。
