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Aldosterone Antagonism Fails to Attenuate Age-Associated Left Ventricular Fibrosis

¹ Division of Kinesiology, Laboratory of Molecular Kinesiology, University of Michigan, Ann Arbor.
² Division of Kinesiology and Health
³ Department of Animal Science, University of Wyoming, Laramie.

Address correspondence to Marvin O. Boluyt, PhD, Division of Kinesiology, Laboratory of Molecular Kinesiology, University of Michigan, 1209 CCRB, 401 Washtenaw Avenue, Ann Arbor, MI 48109-2214. E-mail: boluytm{at}umich.edu

Collagen accumulates disproportionately in cardiac remodeling induced by hypertension and associated with advancing age. Spironolactone (Spiro), an aldosterone antagonist, attenuates the accumulation of collagen induced by hypertension. It was hypothesized that Spiro would attenuate the age-associated increase in percent collagen in the heart. Female Fisher 344 rats at 3 months (Y), 12 months (M), and 21 months (O) of age were treated with Spiro (30 mg/kg/d) or vehicle (Veh) for 2 months, yielding six groups: Y-Veh, Y-Spiro, M-Veh, M-Spiro, O-Veh, and O-Spiro. Hearts were harvested for immunoblotting, RNA blotting, and biochemical analysis. Percent collagen in the left ventricle and septum was greatest in the oldest rats. Spiro did not significantly attenuate the age-associated increase in collagen fraction or the age-associated increases in expression of atrial natriuretic factor and ß-myosin heavy chain messenger RNA. Chronic aldosterone antagonism does not attenuate the age-associated increase in collagen fraction in the female Fisher 344 rat heart.