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Calcium paradox of aldosteronism and the role of the parathyroid glands

Divisions of ¹Cardiovascular Diseases and ²Endocrinology, Department of Medicine, and Departments of ³Surgery and ⁴Obstetrics and Gynecology, University of Tennessee Health Science Center, Memphis, Tennessee

Submitted 20 May 2005 ; accepted in final form 19 August 2005

The hypercalciuria and hypermagnesuria that accompany aldosteronism contribute to a fall in plasma ionized extracellular Ca²⁺ and Mg²⁺ concentrations ([Ca²⁺]_o and [Mg²⁺]_o). Despite these losses and the decline in extracellular levels of these cations, total intracellular and cytosolic free Ca²⁺ concentration ([Ca²⁺]_i) is increased and oxidative stress is induced. This involves diverse tissues, including peripheral blood mononuclear cells (PBMC) and plasma. The accompanying elevation in plasma parathyroid hormone (PTH) and reduction in bone mineral density caused by aldosterone (Aldo)-1% NaCl treatment (AldoST) led us to hypothesize that Ca²⁺ loading and altered redox state are due to secondary hyperparathyroidism (SHPT). Therefore, we studied the effects of total parathyroidectomy (PTx). In rats receiving AldoST, without or with a Ca²⁺-supplemented diet and/or PTx, we monitored urinary Ca²⁺ and Mg²⁺ excretion; plasma [Ca²⁺]_o, [Mg²⁺]_o, and PTH; PBMC [Ca²⁺]_i and H₂O₂ production; plasma ₁-antiproteinase activity; total Ca²⁺ and Mg²⁺ in bone, myocardium, and rectus femoris; and gp91^phox labeling in the heart. We found that 1) the hypercalciuria and hypermagnesuria and decline (P < 0.05) in plasma [Ca²⁺]_o and [Mg²⁺]_o that occur with AldoST were not altered by the Ca²⁺-supplemented diet alone or with PTx; 2) the rise (P < 0.05) in plasma PTH with AldoST, with or without the Ca²⁺-supplemented diet, was prevented by PTx; 3) increased (P < 0.05) PBMC [Ca²⁺]_i and H₂O₂ production, increased total Ca²⁺ in heart and skeletal muscle, and fall in bone Ca²⁺ and Mg²⁺ and plasma ₁-antiproteinase activity with AldoST were abrogated (P < 0.05) by PTx; and 4) gp91^phox activation in right and left ventricles at 4 wk of AldoST was attenuated by PTx. AldoST is accompanied by SHPT, with parathyroid gland-derived calcitropic hormones being responsible for Ca²⁺ overload in diverse tissues and induction of oxidative stress. SHPT plays a permissive role in the proinflammatory vascular phenotype.

aldosterone; magnesium; oxidative and nitrosative stress; parathyroid hormone

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