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血管加压素诱导血管平滑肌细胞内钠离子增加的机制。

Mechanisms of vasopressin-induced increase in intracellular Na+ in vascular smooth muscle cells.

作者信息

Okada K, Ishikawa S, Saito T

机构信息

Department of Medicine, Jichi Medical School, Tochigi, Japan.

出版信息

Am J Physiol. 1991 Dec;261(6 Pt 2):F1007-12. doi: 10.1152/ajprenal.1991.261.6.F1007.

DOI:10.1152/ajprenal.1991.261.6.F1007
PMID:1661077
Abstract

The present study was undertaken to examine the interrelationship between the arginine vasopressin (AVP)-induced dynamic changes in intracellular Ca2+ and Na+ concentrations in cultured rat aortic vascular smooth muscle cells (VSMC) by the direct measurements of intracellular Na+ concentration [( Na+]i), cytosolic free calcium [( Ca2+]i), and intracellular pH (pHi) using fluorescence dyes. AVP increased [Ca2+]i and [Na+]i in a dose-dependent manner; the rise in [Ca2+]i preceded the rise in [Na+]i. Pretreatment with the V1 antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid) 2-(O-methyl)-tyrosine] AVP [( d(CH2)5Tyr(Me)]AVP) completely blocked the effects of AVP on [Ca2+]i and [Na+]i. The V2 agonist 1-desamino-8-D-AVP, DDAVP, did not affect basal [Na+]i or the AVP-induced increase in [Na+]i. Also, Ca(2+)-free solution completely blocked the AVP-induced increase in [Na+]i. Moreover, Ca(2+)-free solution decreased the AVP-induced intracellular acidification and blunted the later AVP-induced intracellular alkalinization. These results therefore indicate that after binding to the V1 receptor AVP increases [Na+]i mediated by the activation of Na(+)-Ca2+ and Na(+)-H+ exchanges in VSMC. All of these cellular events are completely dependent on an increase in cellular Ca2+ uptake produced by AVP.

摘要

本研究旨在通过使用荧光染料直接测量细胞内钠离子浓度([Na⁺]i)、胞质游离钙浓度([Ca²⁺]i)和细胞内pH值(pHi),来检测精氨酸加压素(AVP)诱导的培养大鼠主动脉血管平滑肌细胞(VSMC)内Ca²⁺和Na⁺浓度的动态变化之间的相互关系。AVP以剂量依赖的方式增加[Ca²⁺]i和[Na⁺]i;[Ca²⁺]i的升高先于[Na⁺]i的升高。用V1拮抗剂[1-(β-巯基-β,β-环戊亚甲基丙酸)2-(O-甲基)-酪氨酸]AVP[(d(CH₂)₅Tyr(Me)]AVP预处理可完全阻断AVP对[Ca²⁺]i和[Na⁺]i的作用。V2激动剂1-去氨基-8-D-精氨酸加压素(DDAVP)不影响基础[Na⁺]i或AVP诱导的[Na⁺]i升高。此外,无钙溶液完全阻断了AVP诱导的[Na⁺]i升高。而且,无钙溶液降低了AVP诱导的细胞内酸化,并减弱了随后AVP诱导的细胞内碱化。因此,这些结果表明,AVP与V1受体结合后,通过激活VSMC中的Na⁺-Ca²⁺和Na⁺-H⁺交换来增加[Na⁺]i。所有这些细胞事件都完全依赖于AVP引起的细胞Ca²⁺摄取增加。

相似文献

1
Mechanisms of vasopressin-induced increase in intracellular Na+ in vascular smooth muscle cells.血管加压素诱导血管平滑肌细胞内钠离子增加的机制。
Am J Physiol. 1991 Dec;261(6 Pt 2):F1007-12. doi: 10.1152/ajprenal.1991.261.6.F1007.
2
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Effect of vasopressin on Na+ kinetics in cultured rat vascular smooth muscle cells.血管加压素对培养的大鼠血管平滑肌细胞中钠离子动力学的影响。
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Effect of inhibition of Na+/K(+)-adenosine triphosphatase on vascular action of vasopressin.抑制钠/钾(+)-三磷酸腺苷酶对血管加压素血管作用的影响。
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引用本文的文献

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J Clin Invest. 1993 Oct;92(4):1889-95. doi: 10.1172/JCI116781.
2
Low density lipoprotein enhances the cellular action of arginine vasopressin in rat glomerular mesangial cells in culture.低密度脂蛋白增强精氨酸加压素在培养的大鼠肾小球系膜细胞中的细胞作用。
J Clin Invest. 1994 Jun;93(6):2710-7. doi: 10.1172/JCI117285.
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Br J Pharmacol. 1994 Apr;111(4):1067-72. doi: 10.1111/j.1476-5381.1994.tb14853.x.