Riozzi A, Heagerty A M, Ollerenshaw J D, Swales J D
Clin Sci (Lond). 1987 Jul;73(1):29-32. doi: 10.1042/cs0730029.
The metabolism of phosphoinositides was investigated in erythrocyte membranes of essential hypertensive patients, normotensive offspring of hypertensive patients and matched controls. Measurement of 32P-labelling of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate revealed no differences in the rate of incorporation of the isotope in essential hypertensive patients compared with controls. In the normotensive offspring of essential hypertensive patients there was a highly significant increase in the rate of 32P incorporation (P less than 0.01), compared with matched controls, indicating a higher rate of metabolic turnover in these subjects. These data demonstrate that phosphoinositide metabolism is enhanced in subjects genetically at risk of hypertension, before the blood pressure has risen, but once the blood pressure is established, it is no different from control values. Abnormal phosphoinositide metabolism may be a further manifestation of a genetically determined defect of membrane physicochemical function underlying essential hypertension.
对原发性高血压患者、高血压患者的血压正常后代以及匹配的对照组的红细胞膜中的磷酸肌醇代谢进行了研究。对磷脂酰肌醇4 - 磷酸和磷脂酰肌醇4,5 - 二磷酸的32P标记测量显示,与对照组相比,原发性高血压患者中同位素的掺入率没有差异。与匹配的对照组相比,原发性高血压患者的血压正常后代中32P掺入率显著升高(P小于0.01),表明这些受试者的代谢周转率更高。这些数据表明,在血压升高之前,遗传上有高血压风险的受试者的磷酸肌醇代谢增强,但一旦血压确立,其与对照值并无差异。异常的磷酸肌醇代谢可能是原发性高血压潜在的遗传决定的膜物理化学功能缺陷的进一步表现。