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哺乳动物心肌细胞和血管平滑肌细胞中的钙离子振荡和钙离子波。

Ca(2+)-oscillations and Ca(2+)-waves in mammalian cardiac and vascular smooth muscle cells.

作者信息

Wier W G, Blatter L A

机构信息

Department of Physiology, University of Maryland School of Medicine, Baltimore.

出版信息

Cell Calcium. 1991 Feb-Mar;12(2-3):241-54. doi: 10.1016/0143-4160(91)90024-9.

DOI:10.1016/0143-4160(91)90024-9
PMID:2059996
Abstract

In this article, we review briefly the available theories and data on [Ca2+]i-waves and [Ca2+]i-oscillations in mammalian cardiac and vascular smooth muscles. In addition to our review, we also report: (i) the existence and characterization of rapid agonist-induced [Ca2+]i-waves in cultured vascular smooth muscle cells (A7r5 cells); and (ii a new method for studying rapid [Ca2+]i-waves in mammalian cardiac ventricular cells. In mammalian cardiac muscle several types of Ca(2+)-release from sarcoplasmic reticulum (SR) are known to occur and might be involved in Ca(2+)-waves and Ca(2+)-oscillations: (a) Ca(2+)-induced release of Ca2+, of the type thought to be important in normal excitation-contraction coupling; (b) spontaneous, cyclic release of Ca2+ related to a Ca(2+)-overload of the SR; and (c) Ins(1,4,5)P3-induced Ca(2+)-release. The available data support the idea that [Ca2+]i-waves in heart propagate by a mechanism somewhat different than that involved in normal excitation-contraction coupling (a, above), perhaps involving spontaneous release of Ca2+ from an overloaded SR (b, above). In mammalian vascular smooth muscle, our data support the idea that agonist-receptor interaction (vasopressin, in this case) initiates [Ca2+]i-waves that then propagate via some form of Ca(2+)-induced release of Ca2+, perhaps in a manner similar to that proposed by Berridge and Irvine [1].

摘要

在本文中,我们简要回顾了关于哺乳动物心脏和血管平滑肌中[Ca2+]i波和[Ca2+]i振荡的现有理论和数据。除了我们的综述之外,我们还报告:(i) 培养的血管平滑肌细胞(A7r5细胞)中快速激动剂诱导的[Ca2+]i波的存在及其特征;以及(ii) 研究哺乳动物心室细胞中快速[Ca2+]i波的一种新方法。已知在哺乳动物心肌中会发生几种类型的肌浆网(SR)钙释放,并且可能与钙波和钙振荡有关:(a) 钙诱导的钙释放,这种类型被认为在正常兴奋-收缩偶联中很重要;(b) 与SR钙超载相关的自发周期性钙释放;以及(c) 肌醇-1,4,5-三磷酸(Ins(1,4,5)P3)诱导的钙释放。现有数据支持这样的观点,即心脏中的[Ca2+]i波通过一种与正常兴奋-收缩偶联(上述(a))所涉及的机制略有不同的机制传播,可能涉及从超载的SR中自发释放钙(上述(b))。在哺乳动物血管平滑肌中,我们的数据支持这样的观点,即激动剂-受体相互作用(在这种情况下是血管加压素)引发[Ca2+]i波,然后这些波通过某种形式的钙诱导的钙释放进行传播,其方式可能类似于Berridge和Irvine [1]所提出的方式。

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