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Cardiovascular disease is the leading cause of morbidity and mortality in both men and women, but the incidence for women rises sharply after menopause. This has been mainly attributed in the reduction of the female sex hormone estrogen during menopause, suggesting that estrogen may have cardioprotective effects, although how estrogen exerts its cardioprotective effects is not fully understood. Moreover, the beneficial effect of estrogen on end-organ damage such as cardiac hypertrophy (CH) remains unclear. The aim of the present study was to examine the interaction between estrogen and the natriuretic peptide system (NPS) and their possible roles during the development of CH by using the proANP heterozygous atrial natriuretic peptide (ANP +/−) mouse as a model of salt-sensitive CH. Male, female ANP +/− mice, and also ovariectomized (Ovx) female ANP +/− mice treated with oil or estrogen were fed either a normal or high salt (HS) diet. After a 5-week treatment period, marked CH was noted in the male and oil-injected Ovx female ANP +/− mice treated with HS. The cardiac NPS, i.e. ANP, B-type natriuretic peptide, and natriuretic peptide receptor-A, was activated in these ANP +/− mice. Interestingly, the female and estrogen-injected Ovx female ANP +/− mice did not exhibit CH, and the cardiac NPS remained unchanged. Collectively, we provide direct evidence that estrogen has the ability to resist the induction of salt-induced CH in ANP +/− mice. Furthermore, the development of hypertrophy may be activating the cardiac NPS in an attempt to blunt these structural changes.
