Yamada K, Yoshida S
Department of Clinical Research, Sakura National Hospital, Chiba, Japan.
Am J Physiol. 1991 Jan;260(1 Pt 2):F34-8. doi: 10.1152/ajprenal.1991.260.1.F34.
This study was conducted to determine the involvement of endogenous endothelin (ET), a novel potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system by inhibiting ET action via infusion of a specific ET antiserum at a time of altered sodium balance. Infusion of 1:50 diluted ET antiserum, which completely inhibited renal vasoconstriction by the exogenously administered ET (0.25 to 1.0 nmol/kg), caused an increase in urinary sodium excretion and fractional excretion of sodium and a decrease in plasma renin concentration without significant changes in blood pressure, heart rate, glomerular filtration rate, renal plasma flow, and urine volume compared with the values with nonimmune serum in conscious rats fed a low-salt diet. A time control study showed no significant changes in all parameters. These results suggest that the state of low- compared to high-salt intake causes a relatively stronger activity of endogenous ET, and that the endogenous ET contributes to the adaptative modulations of sodium excretion via renal tubular action and renin release in association with the changed state of sodium balance.
本研究旨在通过在钠平衡改变时输注特异性内皮素抗血清抑制内皮素(ET)作用,来确定这种新型强效血管收缩肽在内源性ET在全身和肾脏血流动力学以及肾素 - 血管紧张素系统中的作用。输注1:50稀释的ET抗血清可完全抑制外源性ET(0.25至1.0 nmol/kg)引起的肾血管收缩,与喂食低钠饮食的清醒大鼠中输注非免疫血清相比,可导致尿钠排泄和钠分数排泄增加,血浆肾素浓度降低,而血压、心率、肾小球滤过率、肾血浆流量和尿量无显著变化。时间对照研究表明所有参数均无显著变化。这些结果表明,与高盐摄入相比,低盐摄入状态会导致内源性ET活性相对增强,并且内源性ET通过肾小管作用和肾素释放,与钠平衡的改变状态相关,有助于钠排泄的适应性调节。