Resink T J, Tkachuk V A, Erne P, Bühler F R
Department of Research, University Hospital, Basel, Switzerland.
J Hypertens Suppl. 1985 Dec;3(3):S37-40.
To determine whether defective calcium-efflux pump activity may be responsible for calcium overload in platelets from patients with essential hypertension, the properties of a calmodulin-stimulated Ca(2+)-ATPase in membranes from 25 normotensive and 27 hypertensive subjects were compared. Calcium-ATPase did not differ in affinity for calmodulin or Ca2+ between groups. Stimulation of Ca(2+)-ATPase activity at saturating calmodulin concentrations is diminished in calmodulin-deficient membranes from established essential hypertensive patients (64%) compared with normotensive subjects (125%) (P < 0.01). The capacity for Ca(2+)-ATPase activity (basal and calmodulin-activated) is markedly greater (1.5 to 1.8-fold) in both native and calmodulin-deficient platelet membranes from hypertensive compared with normotensive subjects. The data suggest that calmodulin-stimulation of Ca(2+)-ATPase in platelets from patients with established essential hypertension does not effectively maintain Ca2+ homeostasis, and that the increased Ca(2+)-ATPase capacity may reflect an adaptation to increased intracellular calcium concentration.
为了确定钙外流泵活性缺陷是否可能导致原发性高血压患者血小板中的钙超载,比较了25名血压正常者和27名高血压患者膜中钙调蛋白刺激的Ca(2+)-ATP酶的特性。两组之间钙ATP酶对钙调蛋白或Ca2+的亲和力没有差异。与血压正常者(125%)相比,已确诊的原发性高血压患者钙调蛋白缺乏的膜中,在饱和钙调蛋白浓度下Ca(2+)-ATP酶活性的刺激降低(64%)(P < 0.01)。与血压正常者相比,高血压患者天然和钙调蛋白缺乏的血小板膜中Ca(2+)-ATP酶活性(基础和钙调蛋白激活)的能力明显更强(1.5至1.8倍)。数据表明,已确诊的原发性高血压患者血小板中钙调蛋白对Ca(2+)-ATP酶的刺激不能有效维持Ca2+稳态,并且Ca(2+)-ATP酶能力的增加可能反映了对细胞内钙浓度增加的一种适应。