It has been proposed that abnormalities in physical properties of the cell membranes may strongly be linked to hypertension and other circulatory disorders. Recent studies have shown that adipokines might actively participate in the pathophysiology of hypertension and in the metabolic syndrome. The purpose of the present article is to elucidate the possible relationships among adipokines, endothelial function, and membrane fluidity (a reciprocal value of membrane microviscosity) of red blood cells (RBCs) in hypertensive and normotensive subjects using an electron spin resonance (ESR) and spin-labeling method. The ESR study demonstrated that membrane fluidity was significantly decreased in hypertensive subjects compared to normotensive subjects. The reduced membrane fluidity of RBCs was associated with decreased levels of plasma nitric oxide (NO)-metabolites and increased levels of plasma asymmetric dimethylarginine (ADMA; an endogenous NO synthase inhibitor), indicating that endothelial function could be a determinant of membrane fluidity of RBCs. Leptin, an adipokine, significantly increased membrane fluidity of RBCs, at least in part, via the NO-dependent mechanism. Furthermore, higher levels of plasma adiponectin were associated with increased membrane fluidity of RBCs. On the other hand, intervention with hormone (estrogen) replacement therapy or administration of benidipine, a Ca channel blocker, significantly improved membrane fluidity of RBCs with a concomitant increase in plasma NO metabolite levels. In this context, it is strongly suggested that both NO and adipokines might have a crucial role in the regulation of rheologic behavior of RBCs and microcirculation in hypertension.
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