Sarah Lindsey, PhD, School of Medicine
Premenopausal females have a lower incidence of many cardiovascular diseases, but this protection steeply declines after menopause. While this trend suggests that endogenous circulating estrogens are advantageous, recent clinical trials failed to show a benefit for hormone replacement therapy. There are two known estrogen receptor subtypes that mediate the genomic actions of the steroid; however, it is not known whether the newly discovered estrogen receptor GPR30 contributes to estrogen’s protective effects. We utilize a unique angiotensin II‐dependent, estrogen‐sensitive, and salt‐sensitive rodent model of hypertension to dissect the mechanisms by which GPR30 mediates its cardiovascular effects. We take an integrative approach by utilizing an in vitro cell culture system, an ex vivo isolated resistance vessel preparation, and in vivo analysis of the congenic mRen2 hypertensive animal to assess the acute and chronic interactions of GPR30 and the renin‐angiotensin system. Information on the role of GPR30 in mediating estrogenic effects may give us information about the cardiovascular benefits and risks of hormone replacement therapy.
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