Intralymphocyte Free Magnesium in Patients With Primary Aldosteronism
Aldosterone and Lymphocyte Magnesium Homeostasis
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Abstract—It is known that hyperaldosteronism has been associated with magnesium deficiency, yet there are no data on the intracellular concentration of ionized magnesium ([Mg2+i]) in subjects with primary aldosteronism (PA). We measured intralymphocyte free magnesium ([Mg2+i]) and intralymphocyte free calcium ([Ca2+i]) in 16 patients with PA and 26 normotensive control subjects (NCs). [Mg2+i] and [Ca2+i] were also measured in blood lymphocytes incubated in vitro with aldosterone, according to a fluorimetric method. In subjects with PA, [Mg2+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, [Ca2+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 [Mg2+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 [Mg2+i] showed an EC50 value of ≈0.5 to 1 nmol/L aldosterone. The reduction in [Mg2+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+-Mg2+ antiporter.
- Received May 5, 1999.
- Revision received June 24, 1999.
- Accepted August 27, 1999.