原发性高血压红细胞钙代谢的初步探讨  

A PRIMARY STUDY ON CALCIUM METABOLISM IN ERYTHROCYTE OF ESSENTIAL HYPERTENSION

作　　者：王玉苓[1] 赵宝昌[1] 顾淑珍[1] 杜国忠[1] 李长育[2] 李桂媛 

机构地区：[1]大连医学院生化教研室 [2]大连医学院第二附属医院内科教研室 [3]大连钢厂医院西门诊

出　　处：《大连医学院学报》1992年第3期48-52,共5页

摘　　要：原发性高血压钙恒稳异常不仅表现在血管平滑肌,也见于其它组织细胞,尤其是血液的有形成分。本文观察了原发性高血压患者红细胞的某些钙恒稳指标,并与正常人进行了比较。结果表明:高血压患者红细胞总钙浓度较正常人明显增加,红细胞膜Ca^(2+)-ATP酶活性明显降低,胞浆钙调素含量显著降低。结果提示:高血压患者红细胞Ca^(2+)-ATP酶活性下降导致胞内Ca^(2+)浓度升高,从而增加外周血管阻力,而CaM可能是通过调节Ca^(2+)-ATP酶活性间接影响血压的。Recent studies showed that the abnormality of calcium homeostasis inessential hypertension was revealed not only in smooth muscular cellsof blood vessel, but also in other tissues and cells, especially in formedelements of the blood. In this study, some indexes of calcium homeo-stasis in red blood cells of hypertensive persons were observed, andcompared with normal controls. The results were showed as follows:the total calcium concentration in red blood cells of essential hypertensivepatients (EHP) was higher than that of normal persons, Ca^(2+)-ATPaseactivity of calmodulin-deficient membrane was decreased significantlyin EHP, and the concentration of CaM in cytoplasma was decreasedsignificantly in EHP. The results suggested that the decreased Ca^(2+)-ATPase activity lead to higher level of cytoplasmic free Ca^(2+) andtherefore increased peripheral vascular resistance, while CaM mayinfluence blood pressure indirectly by regulating the activity of Ca^(2+)-ATPase.

关 键 词：高血压 红细胞 钙代谢 

分 类 号：R543.102[医药卫生—心血管疾病]