{"title":"Decreased cell membrane magnesium in some essential hypertension patients.","authors":"M T Mattingly, W A Brzezinski, I C Wells","doi":"10.3109/10641969109082615","DOIUrl":null,"url":null,"abstract":"<p><p>The concentrations of total ([T-Mg]), ultrafilterable ([UF-Mg]), and protein-bound or nonfilterable ([NF-Mg]) magnesium were measured in the plasma and in the intracellular compartment of blood from 8 essential hypertensive patients and 9 normotensive subjects. In the former, [T-Mg] was unchanged in the plasma but decreased in whole blood due to decreases of both [UF-Mg] and [NF-MG]; [UF-Mg] was increased in plasma but decreased intracellularly while [NF-Mg] was decreased in plasma and unchanged intracellularly. These concentrations correlated significantly with the average blood pressures. Decreased Mg binding to the erythrocyte membrane was also observed in 13 additional essential hypertensive patients. This decreased binding may well be responsible for the decreased intracellular [UF-Mg] in the blood of such patients. The cause of the decreased Mg binding to the erythrocyte membrane is unknown, but the binding is returned to normal by incubating erythrocytes from essential hypertensive patients with blood plasma from normotensive subjects. Decreased Mg binding to cell membranes must also occur in frankly Mg-deficient patients, some of whom, as a consequence of the primary deficiency of this mineral, are hypertensive. Normal Mg binding to erythrocyte membranes was observed in two patients with hypertension indicating that hypertension per se does not cause decreased Mg binding to cell membranes. These observations suggest that decreased Mg binding to cell membranes may be an important contributing factor in some cases of essential hypertension.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"13 1","pages":"65-82"},"PeriodicalIF":0.0000,"publicationDate":"1991-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969109082615","citationCount":"6","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and experimental hypertension. Part A, Theory and practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/10641969109082615","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
Abstract
The concentrations of total ([T-Mg]), ultrafilterable ([UF-Mg]), and protein-bound or nonfilterable ([NF-Mg]) magnesium were measured in the plasma and in the intracellular compartment of blood from 8 essential hypertensive patients and 9 normotensive subjects. In the former, [T-Mg] was unchanged in the plasma but decreased in whole blood due to decreases of both [UF-Mg] and [NF-MG]; [UF-Mg] was increased in plasma but decreased intracellularly while [NF-Mg] was decreased in plasma and unchanged intracellularly. These concentrations correlated significantly with the average blood pressures. Decreased Mg binding to the erythrocyte membrane was also observed in 13 additional essential hypertensive patients. This decreased binding may well be responsible for the decreased intracellular [UF-Mg] in the blood of such patients. The cause of the decreased Mg binding to the erythrocyte membrane is unknown, but the binding is returned to normal by incubating erythrocytes from essential hypertensive patients with blood plasma from normotensive subjects. Decreased Mg binding to cell membranes must also occur in frankly Mg-deficient patients, some of whom, as a consequence of the primary deficiency of this mineral, are hypertensive. Normal Mg binding to erythrocyte membranes was observed in two patients with hypertension indicating that hypertension per se does not cause decreased Mg binding to cell membranes. These observations suggest that decreased Mg binding to cell membranes may be an important contributing factor in some cases of essential hypertension.