发病机制
中枢神经系统
医学
血管舒缩
交感神经系统
原发性高血压
高血压的病理生理学
盐皮质激素
肾素-血管紧张素系统
神经科学
血压
生物信息学
内分泌学
内科学
醛固酮
生物
作者
Michael J. Brody,Kurt J. Varner,Elisardo C. Vasquez,Sarah Lewis
出处
期刊:Hypertension
[Ovid Technologies (Wolters Kluwer)]
日期:1991-11-01
卷期号:18 (5_supplement)
被引量:52
标识
DOI:10.1161/01.hyp.18.5_suppl.iii7
摘要
A large body of evidence indicates that the central nervous system plays an essential role in the pathogenesis of hypertension. However, in many cases the specific brain regions involved and the mechanisms by which these regions promote hypertension are not known. In recent years, research in this and other laboratories has attempted to determine the mechanisms by which neural and humoral signals arising in response to pathological conditions (often occurring in the periphery) interact with the central nervous system to produce hypertension. In this article, we illustrate the coupling of peripheral and central factors in the pathogenesis of hypertension by examining the central actions of angiotensin II and mineralocorticoids in the expression of renal hypertension and mineralocorticoid-salt hypertension, respectively. We also review recent data from this laboratory illustrating the involvement of medullary vasomotor centers in the development of neurogenic hypertension after sinoaortic deafferentation and in the maintenance of hypertension in the spontaneously hypertensive rat.
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