Molecular mechanisms include an activated renin-angiotensin-aldosterone system in response to low estrogen during menopause, the downregulation by estrogen of proteins related to diastolic function, the progesterone activation of the extracellular signal-regulated kinase 2 inducing cardiac hypertrophy during pregnancy, and lower excitation-contraction mediated by calcium and glucose uptake and utilization compared with male (72). This evidence concerns the gene REN and cardiac hypertrophy.