Brent Hill, Ph.D.

Professor and Biology Chair

LSC 180

(501) 450-5915


B.A., Biology, Luther College, 1993

M.S., Veterinary Physiology & Pharmacology, College of Veterinary Medicine, Iowa State University. 1995

Ph.D., Medical Physiology, College of Medicine, University of Missouri, 2000

Started at UCA in 2003

Courses Taught:

Structure & Function of the Human Body I and II

Cardiovascular Physiology

Cell Biology

Regulatory Physiology

Biology for General Education

Research Interests:

The loss of estradiol (e.g., estrogen) with menopause causes a dramatic rise in the development of coronary heart disease. In fact, atherosclerosis of the coronary arteries (i.e., coronary artery/heart disease) is the number one killer of postmenopausal women and is considered, in part, an age-related disease. It has been speculated that the protective effects of estradiol against coronary artery disease may partially be due to theaction of its metabolites. The overall goal of my research is to understand how the metabolites of estradiol may protect against coronary artery disease. As previously established for estradiol, the protective effects of the metabolites will likely be due to its actions on (1) coronary artery tone, and/or (2) smooth muscle cell proliferation. Our objective is to evaluate the most biologically efficacious estradiol metabolites, 2-hydroxyestradiol and 2-methoxyestradiol, at the molecular/cellular level and then determine if these metabolite-induced effects are present at the tissue level. Remarkably, almost nothing is known about the action of these estradiol metabolites on the vasculature; most of the limited data on their influence is related to its antimitogenic effect on cancer cells (e.g., breast cancer). Please contact me if you desire to be an undergraduate researcher or pursue a graduate (M.S.) degree in my laboratory.

Selected Publications:

Hill, B.J.F., R.J. Dalton, B.K. Joseph, K. Thakali, and N.J. Rusch. 17beta-estradiol reduces Cav1.2 channel abundance and attenuates Ca2+-dependent contractions in coronary arteries. Pharmacol Res Perspect, in press, 2017.
Deckard, C., A. Walker, and B.J.F. Hill. Using three-point bending to evaluate tibia bone strength in ovariectomized young mice. J Biol Phys, 2017.
Hill, B.J.F. and E. Muldrew. Oestrogen upregulates the sarcoplasmic reticulum Ca2+-ATPase pump in coronary arteries. Clin Exp Pharmacol Physiol. 41(6):430-6, 2014.
Hill, B.J.F., and W.M. Moran. Biology departments need to increase the integration of physiology into their core curriculum. Journal of College Science Teaching, 41(5): 10-11, 2012.
 Hill, B.J.F., I Goodman, and W.M. Moran. Use of the frog heart preparation to teach students about the spontaneous mechanical activity of the vena cava. Bioscene: Journal of College Biology Teaching, 37(1): 17-22, 2011.
 Hill, B.J.F., S. Gebre, B. Schlicker, R. Jordan, S. Necessary. Nongenomic inhibition of coronary constriction by 17b-estradiol, 2-hydroxyestradiol, and 2-methoxyestradiol. Can J Physiol Pharmacol. 88(2): 147-52, 2010.