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血管紧张素II对血管平滑肌细胞中22Na+转运的影响。

Angiotensin II effect on 22Na+ transport in vascular smooth muscle cells.

作者信息

Kuriyama S, Nakamura A, Hopp L, Fine B P, Kino M, Cragoe E, Aviv A

机构信息

Hypertension Research Unit, University of Medicine and Dentistry of New Jersey, Newark 07103.

出版信息

J Cardiovasc Pharmacol. 1988 Feb;11(2):139-46.

PMID:2452306
Abstract

It is well established that angiotensin II (AII) rapidly increases free cytosolic Ca2+ in vascular smooth muscle cells (VSMCs). Several studies have indicated that the hormone also plays a role in Na+-K+ regulation of these cells. In this study, we explored the mechanism of AII effect on 22Na+ transport in cultured rat VSMCs. The 22Na+ washout from these cells was described by three exponents with exponential factors k1 greater than k2 greater than k3. In 1.8 mM Ca2+ medium, AII (10(-9)-10(-6) M) increased (in a dose response manner) the k1 value, and consequently the initial washout rate constant (kei) for the isotope. AII had no effect on kei in Ca2+-deficient medium or in the presence of ouabain. Amiloride (10(-3) M) and verapamil (10(-5) M) abolished the AII induced increase in kei. These findings are consistent with angiotensin II stimulation of an amiloride-sensitive Na+ transport, which is likely to represent the Na+/H+ antiport. In cultured VSMCs, the sustained stimulation by AII of this transport system requires the presence of extracellular Ca2+ and its influx into these cells.

摘要

众所周知,血管紧张素II(AII)可迅速增加血管平滑肌细胞(VSMC)胞质中的游离Ca2+。多项研究表明,该激素在这些细胞的Na+-K+调节中也发挥作用。在本研究中,我们探讨了AII对培养的大鼠VSMC中22Na+转运的影响机制。这些细胞中22Na+的洗脱由三个指数描述,指数因子k1大于k2大于k3。在1.8 mM Ca2+培养基中,AII(10(-9)-10(-6) M)以剂量反应方式增加k1值,从而增加同位素的初始洗脱速率常数(kei)。AII在缺钙培养基或哇巴因存在下对kei无影响。氨氯地平(10(-3) M)和维拉帕米(10(-5) M)消除了AII诱导的kei增加。这些发现与血管紧张素II刺激氨氯地平敏感的Na+转运一致,这可能代表Na+/H+反向转运体。在培养的VSMC中,AII对该转运系统的持续刺激需要细胞外Ca2+的存在及其流入这些细胞。

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