title: Intralymphocyte free magnesium in patients with primary aldosteronism: aldosterone and lymphocyte magnesium homeostasis.
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 micromol/L, NCs 291+/-43 micromol/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 micromol/L, aldosterone treatment 188+/-39 micromol/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 approximately 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.
authors.affiliation: Departments of Biomedic and Surgical Sciences, University of Verona, Policlinico Borgo Roma, Verona, Italy. delvap@borgoroma.univr.it
authors.forename: P
authors.initials: P
authors.lastname: Delva
authors.forename: C
authors.initials: C
authors.lastname: Pastori
authors.forename: M
authors.initials: M
authors.lastname: Degan
authors.forename: G
authors.initials: G
authors.lastname: Montesi
authors.forename: P
authors.initials: P
authors.lastname: Brazzarola
authors.forename: A
authors.initials: A
authors.lastname: Lechi
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood* / Q000494:pharmacology; D017920:Antiporters / Q000097:blood; D002118:Calcium / Q000097:blood; D002191:Canrenoic Acid / Q000494:pharmacology; D016022:Case-Control Studies; D005260:Female; D006706:Homeostasis; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood* / Q000150:complications; D066298:In Vitro Techniques; D008214:Lymphocytes / Q000187:drug effects / Q000378:metabolism*; D008274:Magnesium / Q000097:blood*; D008275:Magnesium Deficiency / Q000097:blood / Q000150:complications; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology
chemical_list: D017920:Antiporters; D000451:Mineralocorticoid Receptor Antagonists; C046250:sodium-magnesium antiporter; D000450:Aldosterone; D002191:Canrenoic Acid; D008274:Magnesium; D002118:Calcium