Beierwaltes W H
Hypertension Research Division, Henry Ford Hospital, Detroit, Michigan 48202.
Am J Physiol. 1990 May;258(5 Pt 2):F1363-71. doi: 10.1152/ajprenal.1990.258.5.F1363.
Studies were run to determine whether the renal microvascular endothelium influences renin release. Blood-free rat renal cortical slices were incubated in a bicarbonate buffer for 60 min and sampled at 30 and 60 min to determine renin concentration and at 60 min for prostaglandin (PG) E2 and I2 (6-keto-PGF1 alpha) synthesis. Stimulation by 10(-6) M melittin of endogenous PGs simultaneously increased renin release, PGE2, and PGI2 synthesis, and all were inhibited by 1.6 x 10(-6) M meclofenamate. Renin release was stimulated with isoproterenol [26.2 +/- 2.4 ng angiotensin I (ANG I) .h-1.mg-1.30 min-1; P less than 0.001], PGI2 (32.3 +/- 7.4 ng ANG I.h-1.mg-1.mg-1.30 min-1; P less than 0.005), and PGE2 (25.7 +/- 2.8 ng ANG I.h-1.mg-1.30 min-1, P less than 0.001). Acetylcholine did not affect basal renin but potentiated the response to PGE2 by 80% (46.0 +/- 5.8 ng ANG I.h-1.mg-1.30 min-1; P less than 0.001). Atropine (10(-7) M) reversed this potentiation. Deendothelialization of renal microvessels with H2O2 eliminated PGI2, but neither PGE2 nor renin release, and reversed acetylcholine-potentiation of PGE2-stimulated renin release as did meclofenamate. Hemoglobin increased PGE2-stimulated renin similarly to acetylcholine. These studies suggest that stimulating the endothelium with acetylcholine results in selective potentiation of PGE2-stimulated renin release, which may be mediated through some cyclooxygenase product and is independent of endothelium-derived relaxing factor. Thus the renal endothelium may influence or modulate renin release.
开展了多项研究以确定肾微血管内皮是否影响肾素释放。将无血的大鼠肾皮质切片在碳酸氢盐缓冲液中孵育60分钟，并在30分钟和60分钟时取样以测定肾素浓度，在60分钟时取样以测定前列腺素（PG）E2和I2（6-酮-PGF1α）的合成。10（-6）M蜂毒素刺激内源性前列腺素同时增加肾素释放、PGE2和PGI2合成，且所有这些均被1.6×10（-6）M甲氯芬那酸抑制。用异丙肾上腺素刺激肾素释放[26.2±2.4纳克血管紧张素I（ANG I）.小时-1.毫克-1.30分钟-1；P＜0.001]、PGI2（32.3±7.4纳克ANG I.小时-1.毫克-1.毫克-1.30分钟-1；P＜0.005）和PGE2（25.7±2.8纳克ANG I.小时-1.毫克-1.30分钟-1，P＜0.001）。乙酰胆碱不影响基础肾素，但使对PGE2的反应增强80%（46.0±5.8纳克ANG I.小时-1.毫克-1.30分钟-1；P＜0.001）。阿托品（10（-7）M）逆转了这种增强作用。用H2O2使肾微血管去内皮化消除了PGI2，但未消除PGE2和肾素释放，且与甲氯芬那酸一样逆转了乙酰胆碱对PGE2刺激的肾素释放的增强作用。血红蛋白与乙酰胆碱类似地增加了PGE2刺激的肾素。这些研究表明，用乙酰胆碱刺激内皮导致对PGE2刺激的肾素释放的选择性增强，这可能通过某种环氧化酶产物介导且独立于内皮衍生的舒张因子。因此，肾内皮可能影响或调节肾素释放。
