对冷暴露的心血管反应。
Cardiovascular responses to cold exposure.
作者信息
Sun Zhongjie
机构信息
Department of Physiology, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA.
出版信息
Front Biosci (Elite Ed). 2010 Jan 1;2(2):495-503. doi: 10.2741/e108.
Abstract
The prevalence of hypertension is increased in winter and in cold regions of the world. Cold temperatures make hypertension worse and trigger cardiovascular complications (stroke, myocardial infarction, heart failure, etc.). Chronic or intermittent exposure to cold causes hypertension and cardiac hypertrophy in animals. The purpose of this review is to provide the recent advances in the mechanistic investigation of cold-induced hypertension (CIH). Cold temperatures increase the activities of the sympathetic nervous system (SNS) and the renin-angiotensin system (RAS). The SNS initiates CIH via the RAS. Cold exposure suppresses the expression of eNOS and formation of NO, increases the production of endothelin-1 (ET-1), up-regulates ETA receptors, but down-regulates ETB receptors. The roles of these factors and their relations in CIH will be reviewed.
摘要
在冬季以及世界上寒冷地区，高血压的患病率会升高。低温会使高血压病情加重，并引发心血管并发症（中风、心肌梗死、心力衰竭等）。动物长期或间歇性暴露于寒冷环境会导致高血压和心脏肥大。本综述的目的是介绍冷诱导高血压（CIH）机制研究的最新进展。低温会增加交感神经系统（SNS）和肾素-血管紧张素系统（RAS）的活性。交感神经系统通过肾素-血管紧张素系统引发冷诱导高血压。冷暴露会抑制内皮型一氧化氮合酶（eNOS）的表达和一氧化氮（NO）的生成，增加内皮素-1（ET-1）的产生，上调ETA受体，但下调ETB受体。将对这些因素在冷诱导高血压中的作用及其相互关系进行综述。
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