Association of resistin with impaired membrane fluidity of red blood cells in hypertensive and normotensive subjects: an electron paramagnetic resonance study.
Association of resistin with impaired membrane fluidity of red blood cells in hypertensive and normotensive subjects: an electron paramagnetic resonance study.
复制标题
高血压和正常血压受试者抵抗素与红细胞膜流动性受损的关联:电子顺磁共振研究。
DOI:
10.1007/s00380-015-0755-0
复制
发表时间:
2016
影响因子:
1.5
通讯作者:
Kazushi Tsuda
中科院分区:
文献类型:
--
作者:
長谷川由美;難波秀行;櫻井洋一;王堂 哲;Kazushi Tsuda
Abnormalities in physical properties of the cell membranes may strongly be linked to hypertension. Recent evidence indicates that resistin may actively participate in the pathophysiology of insulin resistance, diabetes mellitus, hypertension and other circulatory disorders. The present study was undertaken to investigate the possible relationships among plasma resistin, oxidative stress and membrane fluidity (a reciprocal value of membrane microviscosity) in hypertension. We measured the membrane fluidity of red blood cells (RBCs) in hypertensive and normotensive men using an electron paramagnetic resonance (EPR) and spin-labeling method. The order parameter (S) for the spin-label agents (5-nitroxide stearate) in EPR spectra of red blood cell (RBC) membranes was significantly higher in hypertensive men than in normotensive men, indicating that membrane fluidity was decreased in hypertension. Plasma resistin levels were correlated with systolic blood pressure and 8-iso-prostaglandin F2α levels (an index of oxidative stress). Furthermore, the order parameter (S) of RBCs significantly correlated with plasma resistin and plasma 8-isoPG F2α, suggesting that reduced membrane fluidity of RBCs might be associated with hyperresistinemia and increased oxidative stress. Multivariate regression analysis showed that, after adjustment for confounding factors, plasma resistin might be an independent determinant of membrane fluidity of RBCs. The EPR study suggests that resistin might have a close correlation with impaired rheologic behavior of RBCs and microcirculatory dysfunction in hypertension, at least in part, via an oxidative stress-dependent mechanism.