Zambraski E J, DiBona G F
Am J Physiol. 1976 Oct;231(4):1105-10. doi: 10.1152/ajplegacy.1976.231.4.1105.
Low-level direct renal nerve stimulation increases both renal tubular sodium reabsorption and renal renin secretion rate without changing arterial pressure, glomerular filtration rate, renal blood flow, or intrarenal blood flow distribution. The possibility was considered that intrarenal angiotensin II formation might mediate the antinatriuretic effect by directly enhancing renal tubular sodium reabsorption. Low-level direct renal nerve stimulation was performed in anesthetized saline-loaded dogs before and after intrarenal blockade to angiotensin II with [1-sarcosine, 8-alanine]angiotensin II. The antinatriuretic response to low-level direct renal nerve stimulation was not altered by intrarenal blockade to angiotensin II. Renal renin secretion rate was increased by low-level direct renal nerve stimulation in the absence of changes in systemic or renal hemodynamics. The antinatriuretic effect of low-level direct renal nerve stimulation does not depend on the intrarenal action of angiotensin II.
低水平直接肾神经刺激可增加肾小管钠重吸收和肾素分泌率,而不改变动脉血压、肾小球滤过率、肾血流量或肾内血流分布。研究考虑了肾内血管紧张素II的形成可能通过直接增强肾小管钠重吸收来介导利钠作用的可能性。在用[1-肌氨酸,8-丙氨酸]血管紧张素II对肾内血管紧张素II进行阻断前后,对麻醉状态下输注生理盐水的犬进行低水平直接肾神经刺激。肾内血管紧张素II阻断并未改变低水平直接肾神经刺激的利钠反应。在全身或肾脏血流动力学无变化的情况下,低水平直接肾神经刺激可增加肾素分泌率。低水平直接肾神经刺激的利钠作用不依赖于血管紧张素II的肾内作用。