DIRECT HEMODYNAMIC-EFFECT OF INSULIN IN THE ISOLATED PERFUSED KIDNEY
DIRECT HEMODYNAMIC-EFFECT OF INSULIN IN THE ISOLATED PERFUSED KIDNEY
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DOI：
10.1152/ajprenal.1989.257.4.f580
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发表时间：
1989-10-01
影响因子：
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通讯作者：
STOFF, JS
中科院分区：
文献类型：
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作者：
COHEN, AJ;MCCARTHY, DM;STOFF, JS
在离体灌流肾上观察胰岛素对血流动力学的影响.实验旨在研究激素对基础血流动力学的影响，并在血管紧张素II（ANG II）的存在。生理性胰岛素浓度在基础灌注期引起肾血管舒张和肾小球滤过率（GFR）增加，并减弱ANG II的血管收缩作用，同时限制ANG II诱导的GFR降低。胰岛素也增加了钠重吸收分数，减少了ANG II的利钠利尿作用。虽然需要超生理浓度，但从一开始就输注ANG II的灌注中加入胰岛素会引起肾血管舒张。用高渗白蛋白灌注肾脏以防止滤过，同样证明了胰岛素的血管舒张作用，而不需要肾小球滤过。用吲哚美辛抑制前列腺素（PG）的合成可阻止胰岛素的血管舒张作用。这些数据支持胰岛素通过PG依赖性过程引起肾血管舒张的假设。
The hemodynamic effect of insulin was examined an isolated perfused kidneys. Experiments were designed to study the effect of the hormone on basal hemodynamics and in the presence of angiotensin II (ANG II). Physiological insulin concentrations caused both renal vasodilation and increased glomerular filtration rate (GFR) during basal perfusion periods and attenuated the vasoconstricotr action of ANG II while limiting the ANG II-induced reduction of GFR. Insulin also increased fractional sodium reabsorption and diminished the natriuretic effect of ANG II. The addition of insulin to perfusions in which ANG II was infused from the start caused renal vasodilation, although supraphysiological concentrations were required. Kidneys perfused wihg hyperoncotic albumin to prevent filtration similarly demonstrated a vasodilatory effect of insulin that did not require glomerular filtration. Inhibition of prostaglandin (PG) synthesis with indomethacin prevented the vasodilatory effects of insulin. These data support the hypothesis that insulin causes renal vasodilation by a PG-dependent process.