Intralymphocyte Free Magnesium in Patients With Primary Aldosteronism
- 1 January 2000
- journal article
- Published by Ovid Technologies (Wolters Kluwer Health) in Hypertension
- Vol. 35 (1), 113-117
- https://doi.org/10.1161/01.hyp.35.1.113
Abstract
Abstract —It is known that hyperaldosteronism has been associated with magnesium deficiency, yet there are no data on the intracellular concentration of ionized magnesium ([Mg 2+ i ]) in subjects with primary aldosteronism (PA). We measured intralymphocyte free magnesium ([Mg 2+ i ]) and intralymphocyte free calcium ([Ca 2+ i ]) in 16 patients with PA and 26 normotensive control subjects (NCs). [Mg 2+ i ] and [Ca 2+ i ] were also measured in blood lymphocytes incubated in vitro with aldosterone, according to a fluorimetric method. In subjects with PA, [Mg 2+ i ] was significantly lower than that in NCs (mean±SD; PA 203±56 μmol/L, NCs 291±43 μmol/L, 95% confidence interval 57 to 119, P =0.001). In the patients, [Ca 2+ i ] did not prove to be statistically different from that of NCs (mean±SD; PA 47.2±10.6 nmol/L, NCs 53.2±11 nmol/L). The lymphocytes exposed to the action of aldosterone showed a significant reduction in [Mg 2+ i ] (n=15, NCs 271±28 μmol/L, aldosterone treatment 188±39 μmol/L, P =0.001, 95% confidence interval 57 to 108). The dose-effect curve of aldosterone on [Mg 2+ i ] showed an EC 50 value of ≈0.5 to 1 nmol/L aldosterone. The reduction in [Mg 2+ i ] mediated by aldosterone is antagonized by the receptor inhibitor of aldosterone; it is inhibited by inhibitors of protein synthesis and is not measurable when the lymphocytes are incubated in an Na + -free medium. The data are consistent with the hypothesis that aldosterone affects the cellular homeostasis of magnesium, probably through modification of the activity of the Na + -Mg 2+ antiporter.Keywords
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