心室肌细胞的兴奋-收缩偶联：血管紧张素II的作用

Excitation-contraction coupling in ventricular myocytes: effects of angiotensin II.

作者信息

Barry W H, Matsui H, Bridge J H, Spitzer K W

机构信息

Division of Cardiology, University of Utah Medical School, Salt Lake City 84132, USA.

出版信息

Adv Exp Med Biol. 1995;382:31-9. doi: 10.1007/978-1-4615-1893-8_4.

DOI:10.1007/978-1-4615-1893-8_4

PMID:8540409

Abstract

The effects of the vasoactive peptide angiotensin II (AII) on contractility and excitation-contraction coupling in isolated adult rabbit ventricular myocytes were investigated. In most ventricular myocytes, AII (10(-8) M) induced a significant increase in fractional shortening which was not associated with an increase in the calcium transient measured with indo-1. AII did increase the intracellular pH by approximately 0.2 5 pH units coincident with the positive inotropic effect. Effects of AII on pH and contractility were blocked by inhibitors of Na+/H+ exchange. AII also increased the rate of pHi recovery from intracellular acidosis at pHi values above 6.9. AII was shown not to affect the L-type inward calcium current. However, in an occasional cell, AII was observed to cause a slight increase in the calcium transient. We hypothesize that this response may reflect an increase of calcium influx on the sodium calcium exchanger, as a consequence of an increase in subsarcolemmal sodium concentration resulting from enhanced Na(+)-H+ exchange.

摘要

研究了血管活性肽血管紧张素II（AII）对成年兔离体心室肌细胞收缩性和兴奋-收缩偶联的影响。在大多数心室肌细胞中，AII（10^(-8) M）可使缩短分数显著增加，这与用indo-1测量的钙瞬变增加无关。AII确实使细胞内pH值升高约0.25个pH单位，与正性肌力作用同时出现。AII对pH值和收缩性的影响被Na+/H+交换抑制剂阻断。在细胞内pH值高于6.9时，AII还增加了细胞内酸中毒时pHi的恢复速率。结果表明，AII不影响L型内向钙电流。然而，在偶尔的细胞中，观察到AII可使钙瞬变略有增加。我们推测，这种反应可能反映了由于增强的Na(+)-H+交换导致肌膜下钠浓度增加，从而使钠钙交换体上的钙内流增加。