Eide I, Loyning E, Langård O, Kiil F
Kidney Int. 1975 Sep;8(3):158-65. doi: 10.1038/ki.1975.95.
Ethacrynic acid infused i.v. in anesthetized dogs after inhibiting sympathetic mechanisms of renin release increased renal blood flow rate (RBF) by 54% and practically abolished autoregulation of RBF; renin release increased from 0.8 +/- 0.9 (mean +/- SEM) to 16.4 +/- 3.7 mug/min (P less than 0.05). Without infusion of ethacrynic acid; constriction of the renal artery to a pressure below the range of autoregulation reduced renovascular resistance markedly and renin release rose to 27.2 +/- 5.5 mug/min (P less than 0.05). During arterial constriction, ethacrynic acid had no additional effect on renovascular resistance or renin release averaging 28.4 +/- 6.7 mug/min. Infusion of ethacrynic acid and saline at control pressure increased sodium excretion to about one-half of the filtrate and reduced rein release which did not, however, return to control. Infusion of hypertonic saline during autoregulated vasodilatation induced by arterial constriction had a similar effect, but again renin release continued to exceed control. We propose that ethacrynic acid increases renin release through a hemodynamic mechanism triggered by afferent arteriolar dilation and inhibits renin release by greatly increasing the delivery of sodium to the distal convoluted tubules.
在麻醉犬中,静脉输注依他尼酸抑制肾素释放的交感神经机制后,肾血流量(RBF)增加了54%,并且几乎消除了RBF的自身调节;肾素释放从0.8±0.9(平均值±标准误)增加到16.4±3.7微克/分钟(P<0.05)。在未输注依他尼酸的情况下,将肾动脉收缩至自身调节范围以下的压力会显著降低肾血管阻力,肾素释放增加至27.2±5.5微克/分钟(P<0.05)。在动脉收缩期间,依他尼酸对肾血管阻力或肾素释放没有额外影响,肾素释放平均为28.4±6.7微克/分钟。在对照压力下输注依他尼酸和生理盐水会使钠排泄增加至滤液的约一半,并减少肾素释放,然而,肾素释放并未恢复到对照水平。在动脉收缩诱导的自身调节性血管舒张期间输注高渗盐水也有类似效果,但肾素释放仍然超过对照水平。我们提出,依他尼酸通过入球小动脉扩张触发的血流动力学机制增加肾素释放,并通过大大增加钠向远曲小管的输送来抑制肾素释放。