Yamada K, Yoshida S
Division of Clinical Research and Internal Medicine, Sakura National Hospital, Japan.
J Cardiovasc Pharmacol. 1991;17 Suppl 7:S290-2. doi: 10.1097/00005344-199100177-00082.
This study was conducted to determine the involvement of endogenous endothelin-1 (ET-1), a potent vasoconstricting peptide, in systemic and renal hemodynamics and in the renin-angiotensin system, by inhibiting ET-1 action with an infusion of specific ET-1 antiserum during altered sodium balance. Infusion of 1:50 diluted ET-1 antiserum, which completely inhibited renal vasoconstriction caused by exogenously administered ET-3 (0.25 to 1.0 nmol/kg), increased urinary sodium excretion (UNaV) and fractional excretion of sodium (FENa), and decreased the plasma renin concentration (PRC) without significant changes in blood pressure, heart rate, GFR, RPF, or urine volume (UV) in conscious rats fed a low-salt diet, but not those on a high-salt diet. A time-control study showed no significant changes in any of these parameters. These results suggest that during low salt intake, in comparison to high salt intake, endogenous ET is more potent. Endogenous ET may thus contribute to the adaptive modulation of sodium excretion by a renal tubular action, and of renin release in association with a change in sodium balance.
本研究旨在通过在钠平衡改变期间输注特异性内皮素 -1(ET-1)抗血清来抑制ET-1的作用,从而确定强效血管收缩肽内源性ET-1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-1抗血清可完全抑制外源性给予ET-3(0.25至1.0 nmol/kg)引起的肾血管收缩,增加低盐饮食的清醒大鼠尿钠排泄(UNaV)和钠分数排泄(FENa),并降低血浆肾素浓度(PRC),而血压、心率、肾小球滤过率(GFR)、肾血浆流量(RPF)或尿量(UV)无显著变化,但高盐饮食的大鼠则无此现象。一项时间对照研究表明这些参数均无显著变化。这些结果表明,与高盐摄入相比,低盐摄入时内源性ET作用更强。因此,内源性ET可能通过肾小管作用对钠排泄以及与钠平衡变化相关的肾素释放进行适应性调节。