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Loss of bone minerals and strength in rats with aldosteronism

Divisions of ¹Cardiovascular Diseases and ²Endocrinology, Department of Medicine; and Departments of ³Surgery, ⁴Obstetrics and Gynecology, ⁵Pediatrics, and ⁶Orthopaedic Surgery, University of Tennessee Health Science Center, Memphis, Tennessee 38163

Submitted 25 May 2004 ; accepted in final form 24 June 2004

Congestive heart failure (CHF) is a clinical syndrome with origins rooted in a salt-avid state largely mediated by effector hormones of the circulating renin-angiotensin-aldosterone system. Other participating neurohormones include catecholamines, endothelin-1, and arginine vasopressin. CHF is accompanied by a systemic illness of uncertain causality. Features include the appearance of oxidative/nitrosative stress and a wasting of tissues including bone. Herein we hypothesized that inappropriate (relative to dietary Na⁺) elevations in plasma aldosterone (Aldo) contribute to an altered redox state, augmented excretion of divalent cations, and in turn, a loss of bone minerals and strength. In uninephrectomized rats that received chronic Aldo and 1% NaCl treatment for 4–6 wk, we monitored plasma ₁-antiproteinase activity, which is an inverse correlate of oxidative/nitrosative stress; plasma concentrations of ionized Mg²⁺ and Ca²⁺; urinary Mg²⁺ and Ca²⁺ excretion; and bone mineral composition and strength to flexure stress. Compared with controls, we found reductions in plasma ₁-antiproteinase activity and ionized Mg²⁺ and Ca²⁺ together with persistently elevated urinary Mg²⁺ and Ca²⁺ excretion, a progressive loss of bone mineral density and content with reduced Mg²⁺ and Ca²⁺ concentrations, and a reduction in cortical bone strength. Thus the hypermagnesuria and hypercalciuria that accompany chronic Aldo-1% NaCl treatment contribute to the systemic appearance of oxidative/nitrosative stress and a wasting of bone minerals and strength.

aldosterone; congestive heart failure; peripheral blood mononuclear cells; antiproteinase; parathyroid hormone

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