Carr S J, Sikand K, Moore D, Norman R I
Department of Medicine and Therapeutics, University of Leicester, UK.
J Hypertens. 1995 Jan;13(1):139-46.
To investigate the alterations in erythrocyte ghost membrane microviscosity in essential hypertensive patients and to determine the relationship between these changes and the sodium-lithium countertransport activity as a sensitive marker of membrane function.
Forty-three normolipidaemic essential hypertensive patients (23 treated, 20 untreated) and 27 normotensive controls were studied. Patients were attending the hospital hypertension clinic or a local general practitioner's surgery.
Erythrocyte sodium-lithium countertransport activity was measured. The Michaelis constant (Km) for extracellular sodium and maximal reaction velocity for sodium-lithium countertransport were measured in a subgroup consisting of 22 essential hypertensive patients and 11 normotensive controls. Erythrocyte membrane microviscosity was measured using fluorescence polarization anisotropy of 1,6-diphenyl-1,3,5-hexatriene (DPH) and 1-[4-trimethylammoniumphenyl]-6-phenyl-1,3,5-hexatriene (TMA-DPH).
There was no significant difference in the fluorescence polarization anisotropy of DPH or TMA-DPH between normotensive and essential hypertensive patients. However, the fluorescence polarization anisotropy of TMA-DPH was increased significantly (reflecting increased membrane microviscosity) in hypertensive patients with a family history of hypertension compared with in patients without a family history of hypertension. The standard sodium-lithium countertransport activity was elevated in essential hypertensive patients compared with normotensive controls, and the Km for sodium was significantly lower in patients with a family history of hypertension than in patients without a family history of hypertension. Patients with a family history of hypertension were clustered, with significantly lower Km for sodium and higher TMA-DPH anisotropies than either hypertensive patients without a family history of hypertension or normotensive controls.
These findings suggest that a high membrane microviscosity affecting the outer region of the lipid bilayer is associated with altered sodium-lithium countertransport kinetics in a subgroup of essential hypertensive patients consisting of those with a family history of hypertension.
研究原发性高血压患者红细胞影膜微黏度的变化,并确定这些变化与作为膜功能敏感标志物的钠-锂逆向转运活性之间的关系。
研究了43例血脂正常的原发性高血压患者(23例接受治疗,20例未治疗)和27例血压正常的对照者。患者均在医院高血压门诊或当地全科医生诊所就诊。
测量红细胞钠-锂逆向转运活性。在一个由22例原发性高血压患者和11例血压正常的对照者组成的亚组中,测量细胞外钠的米氏常数(Km)和钠-锂逆向转运的最大反应速度。使用1,6-二苯基-1,3,5-己三烯(DPH)和1-[4-三甲基铵苯基]-6-苯基-1,3,5-己三烯(TMA-DPH)的荧光偏振各向异性来测量红细胞膜微黏度。
血压正常者与原发性高血压患者之间,DPH或TMA-DPH的荧光偏振各向异性无显著差异。然而,与无高血压家族史的患者相比,有高血压家族史的高血压患者TMA-DPH的荧光偏振各向异性显著增加(反映膜微黏度增加)。与血压正常的对照者相比,原发性高血压患者的标准钠-锂逆向转运活性升高,有高血压家族史的患者钠的Km显著低于无高血压家族史的患者。有高血压家族史的患者聚集在一起,其钠的Km显著低于无高血压家族史的高血压患者或血压正常的对照者,而TMA-DPH各向异性则更高。
这些发现表明,在有高血压家族史的原发性高血压患者亚组中,影响脂质双分子层外部区域的高膜微黏度与钠-锂逆向转运动力学改变有关。