Intralymphocyte free magnesium in patients with primary aldosteronism - Aldosterone and lymphocyte magnesium homeostasis

It is known that hyperaldosteronism has been associated with magnesium deficiency, yet there are no data on the intracellular concentration of ionized magnesium ([Mg-i(2+)]) in subjects with primary aldosteronism (PA). We measured intralymphocyte free magnesium ([Mg-i(2+)]) and intralymphocyte free calcium ([Ca-i(2+)]) in 16 patients with PA and 26 normotensive control subjects (NCs). [Mg-i(2+)] and [Ca-i(2+)] were also measured in blood lymphocytes incubated in vitro with aldosterone, according to a fluorimetric method. In subjects with PA, [Mg-i(2+)] was significantly lower than that in NCs (mean+/-SD; PA 203+/-56 mu mol/L, NCs 291+/-43 mu mol/L, 95% confidence interval 57 to 119, P=0.001), In the patients, [Ca-i(2+)] 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-i(2+)] (n=15, NCs 271+/-28 mu mol/L. aldosterone treatment 188+/-39 mu mol/L, P=0.001, 95% confidence interval 57 to 108), The dose-effect curve of aldosterone on [Mg-i(2+)] showed an EC50 value of approximate to 0.5 to 1 nmol/L aldosterone. The reduction in [Mg-i(2+)] 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.