Some cellular events in hypertension - an overview

Touyz, R.M. and Milne, F.J. (1990) Some cellular events in hypertension - an overview. Cardiovascular Journal of South Africa, 1(3),

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Abstract

Essential hypertension is determined by the interaction between three main factors - environmental, genetic and pressure control mechanisms (sympathetic nervous system activity, renin-angiotensin-aldosterone axis, and other endocrine controls. 1 Although the pharmacology and physiology of these complex interactions have been partly clarified, the precise pathophysiological mechanisms of blood pressure regulation are poorly understood, and the fundamental underlying disturbance in essential hypertension remains obscure, Systemic arterial blood pressure is the product of cardiac output and total peripheral resistance.1 Theoretically, hypertension could result from an increased cardiac output or total peripheral resistance or both. In wellestablished hypertension, the major abnormality is a rise in total peripheral resistance due to abnormally reduced arteriolar diameter.J The exact cause of the arteriolar narrowing is unknown, although it is now thought that the tissue involved is most probably vascular smooth musc1e. That hypertension may be associated with alterations in cellular (and specifically vascular smooth-muscle) activity was suggested in 1952 when Tobian and Binion5 reported increased sod ium content of renal arteries in postmortem examinations of hypertensive subjects compared with normotensive controls. Recent data suggest tbat the basic .cause of primary hypertension lies in widespread alterations of cell membrane function, altered regulation of free cytoplasmic calcium (Ca<sup>2</sup>) and abnormal transmembrane cation transport.6 Calcium is one of many fundamental regulators of cellular function. An understanding of the general principles of cellular Ca<sup>2</sup> regulation and its relation to vascular smooth-muscle contractility is pivotal to the pathophysiology of hypertension because many cells, tissues and organs use Ca<sup>2</sup> as a positive intracellular messenger.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Touyz, Professor Rhian
Authors: Touyz, R.M., and Milne, F.J.
College/School:College of Medical Veterinary and Life Sciences > Institute of Cardiovascular and Medical Sciences
Journal Name:Cardiovascular Journal of South Africa
ISSN (Online):1680-0745

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