The hypertensive potential of estrogen: An untold story

Abstract Cardiovascular disease (CVD) are the major cause of morbidity and mortality worldwide. The implication of estrogen in these diseases has been extensively studied. While the vast majority of argue for a cardioprotective role of estrogen in vascular inflammation such as in atherosclerosis, the role of estrogen in hypertension remains far from being resolved. The vasorelaxant effect of estrogen has already been well-established. However, emerging evidence supports a vasoconstrictive potential of the hormone. It has been proposed that estrogen-induced type 1 nitric oxide synthase-1 (nNOS) microenvironment accounts for this apparent contradictory role. Depending on nNOS product, nitric oxide or superoxide, estrogen can induce vasodilation or vasoconstriction. In this review, we discuss the evidence supporting the vasorelaxant effects of estrogen, and molecular players involved. Furthermore, we shed light on recent reports revealing a vasoconstrictive role of estrogen, and speculate on the underlying signaling pathways. In addition, we identify certain factors that can account for the discrepant estrogenic effects. This review emphasizes a yin-yang role of estrogen in regulating blood pressure.