{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:49:29Z","timestamp":1787017769394,"version":"build-2736575974"},"reference-count":44,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p>\n                    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\n                    <jats:sup>+<\/jats:sup>\n                    ) 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\u20136 wk, we monitored plasma \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    -antiproteinase activity, which is an inverse correlate of oxidative\/nitrosative stress; plasma concentrations of ionized Mg\n                    <jats:sup>2+<\/jats:sup>\n                    and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ; urinary Mg\n                    <jats:sup>2+<\/jats:sup>\n                    and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    excretion; and bone mineral composition and strength to flexure stress. Compared with controls, we found reductions in plasma \u03b1\n                    <jats:sub>1<\/jats:sub>\n                    -antiproteinase activity and ionized Mg\n                    <jats:sup>2+<\/jats:sup>\n                    and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    together with persistently elevated urinary Mg\n                    <jats:sup>2+<\/jats:sup>\n                    and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    excretion, a progressive loss of bone mineral density and content with reduced Mg\n                    <jats:sup>2+<\/jats:sup>\n                    and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    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.\n                  <\/jats:p>","DOI":"10.1152\/ajpheart.00477.2004","type":"journal-article","created":{"date-parts":[[2004,10,8]],"date-time":"2004-10-08T22:42:52Z","timestamp":1097275372000},"page":"H2023-H2026","source":"Crossref","is-referenced-by-count":88,"title":["Loss of bone minerals and strength in rats with aldosteronism"],"prefix":"10.1152","volume":"287","author":[{"given":"Vikram S.","family":"Chhokar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Syamal K.","family":"Bhattacharya","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert 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