Chi Y, Gupta R K
Department of Physiology and Biophysics, Albert Einstein College of Medicine of Yeshiva University, Bronx, New York 10461, USA.
Am J Hypertens. 1998 Mar;11(3 Pt 1):340-8. doi: 10.1016/s0895-7061(97)00456-1.
Alterations in fatty acids of membrane phospholipids in essential hypertension may account for altered membrane ion transport, elasticity, and contractility properties of hypertensive tissues. To investigate the abnormalities in membrane fatty acids in essential hypertension, the degree of fatty acid unsaturation ([-CH=CH-]/[-CH3]), the average carbon chain length, ratio of glycerol to fatty acyl chains, ratio of phosphatidylcholine to fatty acyl chains, and the ratio of free and acylated cholesterol to fatty acyl chains in fatty acid fractions of membrane phospholipids of aorta, kidney, and heart were determined in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats by 1H nuclear magnetic resonance (NMR) spectroscopy. The degrees of fatty acid unsaturation in the aorta and the kidney membranes were significantly lower in SHR than in WKY rats (aorta, 0.53+/-0.01 v 0.63+/-0.01, n = 5, P = .01; kidney, 0.70+/-0.01 v 0.84+/-0.03, n = 10, P = .01). No significant difference could be detected in fatty acid unsaturation in heart membranes between these two strains. For aorta, kidney, and heart membranes, the average carbon chain lengths of fatty acid fractions of membrane phospholipids were significantly shorter for SHR than for WKY rats (aorta, 15.1+/-0.2 v 18.3+/-0.7, n = 5, P = .02; kidney, 14.5+/-0.2 v 16.4+/-0.4, n = 10, P = .01; heart, 17.3+/-0.5 v 18.8+/-0.6, n = 10, P = .05). The lower unsaturated fatty acid content in membrane phospholipids of the aorta and the kidney, with concomitant reduction in average chain length, may arise from increased oxidation of fatty acid double bonds in hypertensive tissues and may account, in part, for the increased aortic stiffness and abnormal kidney function associated with essential hypertension. Whether the lower unsaturated fatty acid content and decreased carbon chain length of phospholipid membranes in the aorta and the kidney are a cause or a consequence of the high blood pressure, however, remains unknown.
原发性高血压中膜磷脂脂肪酸的改变可能导致膜离子转运、弹性及高血压组织收缩性的改变。为研究原发性高血压中膜脂肪酸的异常情况,采用氢核磁共振波谱法,测定了自发性高血压大鼠(SHR)和Wistar-Kyoto(WKY)大鼠主动脉、肾脏和心脏膜磷脂脂肪酸组分中的脂肪酸不饱和度([-CH=CH-]/[-CH3])、平均碳链长度、甘油与脂肪酰链的比例、磷脂酰胆碱与脂肪酰链的比例以及游离和酰化胆固醇与脂肪酰链的比例。SHR主动脉和肾脏膜中的脂肪酸不饱和度显著低于WKY大鼠(主动脉:0.53±0.01对0.63±0.01,n = 5,P = 0.01;肾脏:0.70±0.01对0.84±0.03,n = 10,P = 0.01)。这两种品系心脏膜中的脂肪酸不饱和度未检测到显著差异。对于主动脉、肾脏和心脏膜,SHR膜磷脂脂肪酸组分的平均碳链长度显著短于WKY大鼠(主动脉:15.1±0.2对18.3±0.7,n = 5,P = 0.02;肾脏:14.5±0.2对16.4±0.4,n = 10,P = 0.01;心脏:17.3±0.5对18.8±0.6,n = 10,P = 0.05)。主动脉和肾脏膜磷脂中不饱和脂肪酸含量降低,同时平均链长度缩短,可能是由于高血压组织中脂肪酸双键氧化增加所致,这可能部分解释了与原发性高血压相关的主动脉僵硬度增加和肾功能异常。然而,主动脉和肾脏中磷脂膜不饱和脂肪酸含量降低及碳链长度缩短是高血压的原因还是结果,仍不清楚。