PS-C05-12: OMENTIN-1 PREDICTS MEMBRANE FLUIDITY OF RED BLOOD CELLS AND MICROCIRCULATORY FUNCTION IN HYPERTENSIVE SUBJECTS BY THE NITRIC OXIDE-DEPENDENT MECHANISM

Abstract

Objective: It has been shown that abnormalities in physical properties of the cell membranes may strongly be linked to hypertension. Recent evidence indicates that omentin-1, an adipokine with anti-inflammatory properties, may actively participate in the pathophysiology of hypertension, atherosclerosis and other cardiovascular diseases. However, few studies have evaluated the association between omentin-1 and membrane function in hypertension. The present study was performed to investigate possible relationships among omentin-1, endothelial function and membrane fluidity (a reciprocal value of membrane microviscosity) of red blood cells (RBCs) in patients with essential hypertension and normotensive subjects. Design and method: We measured the membrane fluidity of RBCs with an electron spin resonance (ESR) and spin labeling method. In each ESR spectrum, we calculated the order parameter (S) for the spin-label agent (5-nitroxide stearate). The greater the value of the order parameter (S) was, the lower the membrane fluidity of RBC was. Results: (1) The order parameter (S) obtained from the ESR spectra of RBC membranes was significantly greater in hypertensive subjects (0.727 ± 0.001, n = 64) than in normotensive subjects (0.719 ± 0.001, n = 49, P < 0.0001), indicating that membrane fluidity of RBCs might be reduced in hypertensive subjects compared with normotensive subjects. (2) Plasma omentin-1 levels were lower in hypertensive subjects than in normotensive subjects (HT 0.486 ± 0.014 ng/mL, n = 64, NT 0.537 ± 0.019 ng/mL, n = 49, P < 0.05). Plamsa omentin-1 significantly correlated with plasma nitric oxide (NO)-metabolite levels (an index of endothelial function) (r = 0.392, n = 113, P < 0.0001). (3) Furthermore, the order parameter (S) of RBCs inversely correlated with both plasma omentin-1 (r = -0.347, n = 113, P < 0.001) and plasma NO-metabolites, suggesting that reduced membrane fluidity of RBCs might be associated with decreased levels of plasma omentin-1 and endothelial dysfunction. (4) Multivariate regression analysis showed that, after adjusting for confounding factors, plasma omentin-1 might be an independent predictor of membrane fluidity of RBCs. Conclusions: The ESR study demonstrated that lower plasma omentin-1 levels might have a close correlation with reduced membrane fluidity of RBCs and impaired hemorheologic behavior in hypertensive subjects by the NO-dependent mechanism. It is strongly suggested that plasma omentin-1 could be a putative biomarker for the microcirculatory function in hypertension.