This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Delva, P. Articles by Lechi, A. Search for Related Content PubMed PubMed Citation Articles by Delva, P. Articles by Lechi, A. Related Collections Ion channels/membrane transport Other etiology

(Hypertension. 2000;35:113.)
© 2000 American Heart Association, Inc.

Scientific Contributions

Intralymphocyte Free Magnesium in Patients With Primary Aldosteronism

Aldosterone and Lymphocyte Magnesium Homeostasis

Pietro Delva; Caterina Pastori; Maurizio Degan; Germana Montesi; Paolo Brazzarola; Alessandro Lechi

From the Departments of Biomedic and Surgical Sciences (P.D., C.P., M.D., G.M., A.L.) and Surgery (P.B.), University of Verona, Policlinico Borgo Roma, Verona, Italy.

Correspondence to Dr Pietro Delva, Medicina Interna C, Università di Verona, Policlinico Borgo Roma, 37134 Verona, Italy. E-mail delvap{at}borgoroma.univr.it

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.

Key Words: aldosterone • ions • magnesium • calcium • lymphocytes • hypertension

This article has been cited by other articles:

				Y. Sun, R. A. Ahokas, S. K. Bhattacharya, I. C. Gerling, L. D. Carbone, and K. T. Weber Oxidative stress in aldosteronism Cardiovasc Res, July 15, 2006; 71(2): 300 - 309. [Abstract] [Full Text] [PDF]

				V. S. Chhokar, Y. Sun, S. K. Bhattacharya, R. A. Ahokas, L. K. Myers, Z. Xing, R. A. Smith, I. C. Gerling, and K. T. Weber Hyperparathyroidism and the Calcium Paradox of Aldosteronism Circulation, February 22, 2005; 111(7): 871 - 878. [Abstract] [Full Text] [PDF]

				Y. He, G. Yao, C. Savoia, and R. M. Touyz Transient Receptor Potential Melastatin 7 Ion Channels Regulate Magnesium Homeostasis in Vascular Smooth Muscle Cells: Role of Angiotensin II Circ. Res., February 4, 2005; 96(2): 207 - 215. [Abstract] [Full Text] [PDF]

				R. A. Ahokas, Y. Sun, S. K. Bhattacharya, I. C. Gerling, and K. T. Weber Aldosteronism and a Proinflammatory Vascular Phenotype: Role of Mg2+, Ca2+, and H2O2 in Peripheral Blood Mononuclear Cells Circulation, January 4, 2005; 111(1): 51 - 57. [Abstract] [Full Text] [PDF]

				V. S. Chhokar, Y. Sun, S. K. Bhattacharya, R. A. Ahokas, L. K. Myers, Z. Xing, R. A. Smith, I. C. Gerling, and K. T. Weber Loss of bone minerals and strength in rats with aldosteronism Am J Physiol Heart Circ Physiol, November 1, 2004; 287(5): H2023 - H2026. [Abstract] [Full Text] [PDF]

				K. T. Weber Furosemide in the long-term management of heart failure: The good, the bad, and the uncertain J. Am. Coll. Cardiol., September 15, 2004; 44(6): 1308 - 1310. [Full Text] [PDF]

				K. T. Weber From Inflammation to Fibrosis: A Stiff Stretch of Highway Hypertension, April 1, 2004; 43(4): 716 - 719. [Full Text] [PDF]

				R. A. Ahokas, K. J. Warrington, I. C. Gerling, Y. Sun, L. A. Wodi, P. A. Herring, L. Lu, S. K. Bhattacharya, A. E. Postlethwaite, and K. T. Weber Aldosteronism and Peripheral Blood Mononuclear Cell Activation: A Neuroendocrine-Immune Interface Circ. Res., November 14, 2003; 93 (10): e124 - e135. [Abstract] [Full Text] [PDF]

				K. T Weber, Yao Sun, L. A Wodi, A. Munir, E. Jahangir, R. A Ahokas, I. C Gerling, A. E Postlethwaite, and K. J Warrington Toward a broader understanding of aldosterone in congestive heart failure Journal of Renin-Angiotensin-Aldosterone System, September 1, 2003; 4(3): 155 - 163. [Abstract] [PDF]

				I. C. Gerling, Y. Sun, R. A. Ahokas, L. A. Wodi, S. K. Bhattacharya, K. J. Warrington, A. E. Postlethwaite, and K. T. Weber Aldosteronism: an immunostimulatory state precedes proinflammatory/fibrogenic cardiac phenotype Am J Physiol Heart Circ Physiol, July 11, 2003; 285(2): H813 - H821. [Abstract] [Full Text] [PDF]

				Y. Sun, J. Zhang, L. Lu, S. S. Chen, M. T. Quinn, and K. T. Weber Aldosterone-Induced Inflammation in the Rat Heart : Role of Oxidative Stress Am. J. Pathol., November 1, 2002; 161(5): 1773 - 1781. [Abstract] [Full Text] [PDF]

				R. M. Touyz, C. Mercure, and T. L. Reudelhuber Angiotensin II Type I Receptor Modulates Intracellular Free Mg2+ in Renally Derived Cells via Na+-dependent Ca2+-independent Mechanisms J. Biol. Chem., April 20, 2001; 276(17): 13657 - 13663. [Abstract] [Full Text] [PDF]