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平滑肌的钙调节与收缩功能障碍

Calcium regulation and contractile dysfunction of smooth muscle.

作者信息

Sakai Y, Kwan C Y

机构信息

Department of Physiology, School of Medicine, Showa University, Tokyo, Japan.

出版信息

Biol Signals. 1993 Sep-Oct;2(5):305-12. doi: 10.1159/000109511.

Abstract

A brief overview of recent findings of abnormal contractile function of smooth muscle under several selected pathophysiological conditions is presented and related to the dysfunction of the control of cytosolic calcium ion concentration, [Ca2+]. In diabetes mellitus (DM), contractile abnormalities depend on the animal species, vascular segments, mode of the induction of DM, and the period after the induction of DM. The abnormal contractile responses are frequently related to altered Ca2+, membrane transduction and the production and action of intracellular second messengers. The hypertensitive and/or hyperreactive contractile responses of airway smooth muscle in asthma inflammation represent a complex chronic consequence of actions of many cells and mediators. Chronic asthmatic disease seems to be associated with altered Ca2+ handling via changes in gene coding for receptors, enzymes and regulatory proteins, thus contributing to abnormal responsiveness and cell growth. Similarly, changes of contractile function of vascular smooth muscle commonly observed in chronic hypertension have long been recognized to be intimately associated with abnormal handling of Ca2+ at the level of subcellular membranes, isolated cells and intact vascular tissues. However, the subcellular sites of membrane abnormalities remain disputable.

摘要

本文简要概述了在几种选定的病理生理条件下平滑肌收缩功能异常的最新研究结果,并将其与胞质钙离子浓度[Ca2+]调控功能障碍相关联。在糖尿病(DM)中,收缩异常取决于动物种类、血管段、DM诱导方式以及DM诱导后的时间。异常的收缩反应通常与Ca2+改变、膜转导以及细胞内第二信使的产生和作用有关。哮喘炎症中气道平滑肌的高血压和/或高反应性收缩反应是许多细胞和介质作用的复杂慢性后果。慢性哮喘疾病似乎与通过受体、酶和调节蛋白编码基因的变化而改变的Ca2+处理有关,从而导致异常反应性和细胞生长。同样,长期以来人们一直认为,在慢性高血压中常见的血管平滑肌收缩功能变化与亚细胞膜、分离细胞和完整血管组织水平上Ca2+的异常处理密切相关。然而,膜异常的亚细胞位点仍存在争议。

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