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1-脒基精氨酸加压素诱导大鼠利尿钠的机制。

Mechanism of 1-deamino-arginine vasotocin induced natriuresis in rats.

机构信息

Sechenov Institute of Evolutionary Physiology and Biochemistry of the Russian Academy of Sciences, Thorez Av 44, St Petersburg 194223, Russia.

出版信息

Gen Comp Endocrinol. 2011 Feb 1;170(3):460-7. doi: 10.1016/j.ygcen.2010.10.020. Epub 2010 Nov 2.

DOI:10.1016/j.ygcen.2010.10.020
PMID:21050856
Abstract

1-Deamino-arginine vasotocin (1dAVT) induced diuresis and a considerable increase in urinary sodium excretion in female Wistar rats. Sodium fractional excretion rose up to 19.3 ± 1.1%. An increase in urine flow rate after 1dAVT (0.5 nmol/kg body-weight [bw]) injection was accompanied by a significant rise of the solute-free water reabsorption. The 1dAVT-induced natriuresis was as high as natriuresis produced by injection of a maximal dose of furosemide (10mg/kg bw). V(1)-receptor antagonists (ОРС-21268, [β-mercapto-β,β-cyclopentamethylenepropionyl(1),O-Me-Tyr(2),Arg(8)]-vasopressin) blocked the increase in urinary sodium excretion after the 1dAVT injection. The 1dAVT-induced natriuresis was strongly correlated with an increase in the urinary cGMP and prostaglandin E(2) excretion. The natriuretic effect of 1dAVT did not depend on the formation of nitric oxide (NO) or atrial natriuretic peptide of which concentration in the rat blood serum remained stable. The above results indicate that the 1dAVT has unique effects on rat kidney compared to all other known diuretics - it induces extremely high natriuresis and stimulates solute-free water reabsorption. Mechanism of the natriuretic effect of 1dAVT includes decrease in tubular sodium reabsorption due to activation of V(1)-like receptors and formation of cGMP and PGЕ(2).

摘要

1-脒基精氨酸加压素(1dAVT)可诱导雌性 Wistar 大鼠利尿和尿钠排泄显著增加。钠分数排泄率上升至 19.3±1.1%。1dAVT(0.5nmol/kg 体重[bw])注射后尿液流量增加,同时溶质自由水重吸收显著增加。1dAVT 引起的利尿作用与注射最大剂量呋塞米(10mg/kg bw)引起的利尿作用一样高。V1-受体拮抗剂(ОРС-21268,[β-巯基-β,β-环戊二烯甲基丙酰基(1),O-Me-Tyr(2),Arg(8)]-加压素)可阻断 1dAVT 注射后尿钠排泄增加。1dAVT 引起的利尿作用与尿 cGMP 和前列腺素 E2 排泄增加密切相关。1dAVT 的利尿作用不依赖于一氧化氮(NO)或心钠肽的形成,其在大鼠血清中的浓度保持稳定。上述结果表明,与所有其他已知利尿剂相比,1dAVT 对大鼠肾脏具有独特的作用-它可引起极高的利尿作用并刺激溶质自由水重吸收。1dAVT 利尿作用的机制包括通过激活 V1 样受体和形成 cGMP 和 PGЕ(2)来减少肾小管钠重吸收。

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