Vascular smooth muscle membrane in hypertension.

Vascular smooth muscle membrane in hypertension.
复制标题

DOI:
10.1146/annurev.pa.28.040188.002133
复制
发表时间:
1988
影响因子:
12.5
通讯作者:
D. Bohr;R. Webb
D. Bohr;R. Webb
中科院分区:
医学1区
文献类型:
--
作者:
D. Bohr;R. Webb

文献摘要

被引文献

相似文献

这篇文章的标题有很大不同的影响,根据读者的角度来看:临床医生需要知道什么细胞膜与动脉压升高;药理学家想知道这个膜的功能异常;和基本的生物学家是好奇这些功能异常是否可以解释为已知的差异在分子水平上。为了使我们的呼吁具有全球性,我们努力处理这三个关切中的每一个。高血压的动脉压升高通常是由总外周阻力增加引起的,并且高血压患者对标准升压刺激的升压反应的幅度一致地大于正常。从理论和应用的角度来看,了解不同类型高血压之间是否存在导致这些异常的机制差异是很重要的。在一个层面上,所有类型的高血压都是相同的,因为所有类型的高血压都是动脉压和血管反应性升高。然而,在实验性高血压中很明显,遗传性、肾性和盐皮质激素性高血压的起始因素是完全不同的。相关的问题是从引发因素到最终共同结果的一系列事件之间的关系。这些事件在哪里汇合?从目前综述的观点来看,重要的是要问是否所有类型的高血压都是由相同的血管变化引起的。在某种程度上,这个问题可以得到令人信服的肯定回答。在所有类型的高血压中,阻力血管的壁都比正常的厚。Folkow(1)已经确定,这种特性不仅通过以下方式增加血管阻力:
The title of this article has implications that differ greatly according to the reader's perspective: The clinician needs to know what the cell membrane has to do with elevated arterial pressure; the pharmacologist would like to know about functional abnormalities in this membrane; and the basic biologist is curious about whether these functional abnormalities can be accounted for by known differences at a molecular level. In an attempt to be global in our appeal, we have tried to address each of these three concerns. The elevated arterial pressure of hypertension is usually caused by an increased total peripheral resistance, and the magnitude of a pressor response to a standard pressor stimulus is uniformly greater than normal in hyperten­ sion. For both theoretical and applied reasons, it is important to know whether there are mechanistic differences responsible for these abnormalities among the various types of hypertension. At one level, all types of hypertension are the same in that in all of them arterial pressure and vascular responsiveness are elevated. Yet, as is evident in experimental hypertension, the initiating factors for genetic, renal, and mineralocorticoid hypertensions are entirely different. The relevant question is the relationship of sequences of events leading from the initiating factors to the final common outcomes. Where do these events converge? From the point of view of the current review it is important to ask whether all types of hypertension result from the same vascular changes. At one level this question can be given a convincing affirmative answer. In all types of hypertension, resistance vessels have walls that are thicker than normal. Folkow (1) has established that this characteristic not only increases vascular resistance by