Touyz R M, Milne F J, Reinach S G
Department of Medicine, University of Witwatersrand Medical School, Johannesburg, South Africa.
J Hypertens. 1992 Jun;10(6):571-8. doi: 10.1097/00004872-199206000-00010.
To assess the relationship between intracellular Mg2+, Ca2+, Na+ and K+ and cell membrane adenosine triphosphatase (ATPase) activity in normotensive and hypertensive blacks.
Intracellular cations and cell membrane ATPase activity were studied in black patients with untreated essential hypertension and age-, weight- and height-matched normotensive controls. Platelet, erythrocyte and serum Mg2+, Ca2+, Na+ and K+ levels as well as platelet and erythrocyte membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activities were measured in all subjects.
Intracellular Na+ and K+ were measured by flame photometry and Mg+ and Ca+ by atomic absorption spectrophotometry. Cell membrane ATPase activity was determined by a colorimetric method.
The hypertensive group consistently demonstrated depressed activity of each ATPase studied, with significantly lower serum Mg2+, serum K+, erythrocyte Mg2+ and platelet Mg2+ levels compared with the normotensive group. Platelet Na+ and Ca2+ and erythrocyte Ca2+ were significantly elevated in the hypertensive group. In the hypertensive group, mean arterial pressure (MAP) was inversely correlated with platelet and erythrocyte membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase. Serum Mg2+, serum Ca2+ and platelet Mg2+ were negatively correlated with MAP in the hypertensive group whilst erythrocyte and platelet Ca2+ were positively correlated. In the normotensive group, platelet Mg2+ and MAP were negatively, and erythrocyte Ca2+ and MAP, positively correlated.
Black patients with essential hypertension have widespread depression of cell membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activities with serum and intracellular Mg2+ depletion and cytosolic Na+ and Ca2+ overload, which may reflect an underlying membrane abnormality in essential hypertension. These cellular abnormalities may be related to the defective transport mechanisms that in turn may be aggravated by Mg2+ depletion.
评估血压正常和高血压黑人细胞内镁离子（Mg2+）、钙离子（Ca2+）、钠离子（Na+）和钾离子（K+）与细胞膜三磷酸腺苷酶（ATP酶）活性之间的关系。
对未经治疗的原发性高血压黑人患者以及年龄、体重和身高匹配的血压正常对照者进行细胞内阳离子和细胞膜ATP酶活性研究。测量了所有受试者的血小板、红细胞和血清中的Mg2+、Ca2+、Na+和K+水平，以及血小板和红细胞膜上的Na+，K(+)-ATP酶、Ca(2+)-ATP酶和Mg(2+)-ATP酶活性。
通过火焰光度法测量细胞内Na+和K+，通过原子吸收分光光度法测量Mg+和Ca+。采用比色法测定细胞膜ATP酶活性。
高血压组所研究的每种ATP酶活性均持续降低，与血压正常组相比，血清Mg2+、血清K+、红细胞Mg2+和血小板Mg2+水平显著降低。高血压组血小板Na+和Ca2+以及红细胞Ca2+显著升高。在高血压组中，平均动脉压（MAP）与血小板和红细胞膜上的Na+，K(+)-ATP酶、Ca(2+)-ATP酶和Mg(2+)-ATP酶呈负相关。高血压组中血清Mg2+、血清Ca2+和血小板Mg2+与MAP呈负相关，而红细胞和血小板Ca2+与MAP呈正相关。在血压正常组中，血小板Mg2+与MAP呈负相关，红细胞Ca2+与MAP呈正相关。
原发性高血压黑人患者存在细胞膜Na+，K(+)-ATP酶、Ca(2+)-ATP酶和Mg(2+)-ATP酶活性广泛降低，伴有血清和细胞内Mg2+耗竭以及细胞溶质Na+和Ca2+过载，这可能反映了原发性高血压潜在的膜异常。这些细胞异常可能与转运机制缺陷有关，而Mg2+耗竭可能会进一步加重这种缺陷。
