Remmal A, Koutouzov S, Girard A, Meyer P, Marche P
INSERM U7, Department of Pharmacology, Hôpital Necker, Paris, France.
Experientia. 1988 Feb 15;44(2):133-7. doi: 10.1007/BF01952196.
An increase in free cytosolic calcium content has been reported in essential hypertension. Since within the membrane, the phosphoinositides participate in the control of cell calcium homeostasis, we investigated whether impaired phosphoinositide metabolism could account for the calcium handling abnormality observed in hypertensives. In erythrocyte membranes of hypertensives the activity of kinases involved in polyphosphoinositide formation appears to be impaired and could be related to the alteration in calcium handling binding capacity and ATP-dependent calcium transport. In platelets of hypertensives, the hyperactivity of phospholipase C (observed even in the absence of calcium in the external medium) is likely to be responsible for the hypersensitivity of cells to various agonists. These observations are consistent with the hypothesis that in cells from hypertensives, a membrane defect linked to phosphoinositide metabolism is involved in the overall calcium handling defect.
据报道，原发性高血压患者细胞溶质游离钙含量会增加。由于在细胞膜内，磷酸肌醇参与细胞钙稳态的控制，我们研究了磷酸肌醇代谢受损是否可解释高血压患者中观察到的钙处理异常。在高血压患者的红细胞膜中，参与多磷酸肌醇形成的激酶活性似乎受损，这可能与钙处理结合能力和ATP依赖性钙转运的改变有关。在高血压患者的血小板中，磷脂酶C的活性过高（即使在细胞外培养基中没有钙的情况下也可观察到）可能是细胞对各种激动剂过敏的原因。这些观察结果与以下假设一致：在高血压患者的细胞中，与磷酸肌醇代谢相关的膜缺陷参与了整体钙处理缺陷。
