Plasma Membrane in Hypertension: Microviscosity and Calcium Stabilization.

Abstract

Over the past decade the possibility of membrane abnormalities in hypertension has been studied very extensively. These studies reflect the putative significance of membrane abnormalities in the pathogenesis of this disease, and the need for resolution of the great divergence of the results that have been reported. Nevertheless, two sound generalizations have emerged from studies of the plasma membrane in hypertension:1) The microviscosity of the plasma membrane is elevated (fluidity is decreased). However, genetic studies have cast doubt on the possibility that the decreased fluidity of the plasma membrane plays a role in the cause of experimental hypertension.2) The stabilizing influence of calcium is diminished. The roles, if any, of these two abnormalities in the pathogenesis of hypertension require further study. Specific abnormalities, such as that of the Na/Li countertransport or Na/H exchange activity, may be useful phenotypic markers of subgroups of patients with essential hypertension. (Hypertens Res 1994; 17: 79-86) Key Words: cell membrane, membrane microviscosity, ion transport, lipid bilayer, calcium, spontaneously hypertensive rat Plasma membrane abnormalities have been associated with both experimental and clinical hypertension (1,2). The aim of this review is to summarize observations that characterize these abnormalities. It will be evident that the findings do not yet permit comfortable generalizations about the role, if any, played by the membrane abnormalities as a cause of hypertension. Furthermore, current literature includes serious controversies about the characterizations of the membrane abnormalities. Sodium Plasma membrane transport systems for sodium in hypertension received early attention. This interest followed recognition that the blood pressure in hypertension could be manipulated by changes in sodium intake (3) . It was also known that the hypertensive patient responded to a sodium load with an exaggerated natriuresis (4). Something seemed different about sodium metabolism in hypertension.Since it was also recognized that the blood pressure elevation resulted from vasoconstriction that increased total peripheral resistance (TPR), initial studies dealing with an abnormality in sodium metabolism were carried out on vascular smooth muscle in experimental hypertension. Forty years ago Tobian and Binion (5) studying renal and mineralocorticoid hypertension in rats observed an increase in sodium and water in the arteries of these animals. They introduced the concept of water-logging of the vessel wall as contributing to the increase in total peripheral resistance. Definitive studies were then carried out in the tail artery by Friedman (6) and the rat aorta by Jones (7). These studies (7) indicated that the permeability of the plasma membrane of vascular smooth muscle to sodium is increased in mineralocorticoid hypertension and in spontaneously hypertensive rats (SHR).New dimensions of interest arose in the membrane permeability to sodium when Postnov (8) reported that this param...

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