Abstract

Both mechanical load and humoral factors stimulate cardiomyocyte hypertrophy. Mineralocorticoid receptor (MR) antagonists are anti-hypertensive and anti-hypertrophic. Separating the direct myocardial effects from the anti-hypertensive effects is difficult. In normal animals, cardiac effects of aldosterone are not seen in the absence of salt loading. Hypothesis: In the presence of fixed pressure overload (PO), concomitant MR activation leads to “pathologic” hypertrophy and diastolic dysfunction. Methods: 8 week old male mice (FVB background) underwent sham procedure, transverse aortic constriction (TAC) or TAC plus high dose deoxycorticosterone acetate (TAC+DOCA) with normal salt diet for 14 days.

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