- Bachelor of Arts in Psychology: University of Mississippi, Oxford, MS (1999)
- Master of Science in Molecular Biopsychology: University of Memphis, Memphis, TN (2000)
- Doctor of Philosophy in Pharmacology: Louisiana State University Health Sciences Center, New Orleans, LA (2007)
- Postdoctoral Fellowship: Laboratory of Dr. Mark Chappell, Hypertension and Vascular Research Center, Wake Forest School of Medicine, Winston-Salem, NC (2007-2010)
- Instructor: Department of Surgical Sciences, Hypertension and Vascular Research Center, Wake Forest School of Medicine, Winston-Salem, NC (2010-12)
- Assistant Professor: Department of Pharmacology, Tulane University School of Medicine, New Orleans, Louisiana (2012-present).
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.