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Endocrinology Vol. 141, No. 5 1901-1904
Copyright © 2000 by The Endocrine Society

ARTICLES

Sodium-Induced Cardiac Aldosterone Synthesis Causes Cardiac Hypertrophy

Yoshiyu Takeda, Takashi Yoneda, Masashi Demura, Isamu Miyamori and Hiroshi Mabuchi

Second Department of Internal Medicine (Y.T., T.Y., M.D., H.M.), Department of Health Sciences (Y.T.), School of Medicine, Kanazawa University, Kanazawa 920, Japan; and Third Department of Internal Medicine (I.M.), Fukui Medical School, Fukui 910-11, Japan

Address all correspondence and requests for reprints to: Yoshiyu Takeda, Kanazawa University School of Medicine, 2nd Department of Medicine, 13-1 Takara-Machi, Kanazawa 920, Japan.

ABSTRACT

High sodium intake causes cardiac hypertrophy independently of increases in blood pressure. Aldosterone is synthesized in extra- adrenal tissues such as blood vessels, brain, and heart. Effects of 8 weeks of high sodium intake on cardiac aldosterone synthesis, as well as cardiac structure, mass, and aldosterone production, levels of mRNA coding for aldosterone synthase (CYP11B2) and the angiotensin II AT 1 receptor, were studied in normotensive Wistar-Kyoto (WKY) rats. Isolated rat hearts were perfused for 2 hr, and the perfusate was analyzed by high-performance liquid chromatography and mass spectrometry. Aldosterone synthase activity was estimated from the conversion of [14C]deoxycorticosterone to [14C]aldosterone. Levels of mRNA for CYP11B2 and AT 1 receptor were determined by competitive polymerase chain reactions. A high sodium intake for 8 weeks produced left ventricular hypertrophy without elevation of blood pressure. Plasma aldosterone concentrations and plasma renin concentrations were decreased by high sodium intake. Aldosterone production, activity of aldosterone synthase, and expression of mRNA for CYP11B2 and AT 1 receptor were increased in hearts of rats with high sodium intake. These results suggest that high sodium intake increases cardiac aldosterone synthesis, which may contribute to cardiac hypertrophy independently of the circulating renin-angiotensin-aldosterone system.




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