Jane F. Reckelhoff, Ph.D.

Department of Physiology & Biophysics
Room number R618
PHONE: (601) 984-1819
FAX: (601) 984-1817

Areas of Expertise

Gender and hypertension
Renal physiology Gender and renal injury
Hypertension in post-menopausal women
Oxidative stress and the renin-angiotensin system

Techniques

Glomerular & tubular micropuncture; molecular biology; cell culture chronically instrumented rats; immunohistochemistry.

Research Summary

Men are generally at greater risk for cardiovascular disease than are premenopausal women, particularly with regard to enhanced progression of hypertension and loss of renal function. Despite these gender differences in the progression of hypertension and renal disease in man and animals, the mechanisms responsible are unknown. Our current research is involved with the mechanisms by which sex steroids affect blood pressure and renal hemodynamics. We have evidence that androgens, the renin-angiotensin system and oxidative stress all play important roles in the higher blood pressure in males and in the kidney damage associated with hypertension. The mechanisms by which androgens could increase blood pressure are not known. We hypothesize that androgens increase arterial pressure by causing a hypertensive shift in the pressure-natriuresis relationship either by having a direct effect to increase proximal tubular sodium and water reabsorption or by activation of the renin-angiotensin system (RAS). We also hypothesize that the enhanced proximal tubular reabsorption leads to a tubulo-glomerular feedback-mediated afferent vasodilation which in combination with the increase in arterial pressure results in glomerular hypertension and renal injury. Blockade of the RAS prevents the increase in BP in with testosterone.

As mentioned, men are at risk for cardiovascular disease compared to premenopausal women. However, after menopause, BP in women increases until they exhibit greater incidence of hypertension than do men. There is controversy regarding the whether hormone replacement therapy (HRT) reduces blood pressure in post-menopausal women. Most 24 hr ambulatory blood pressure monitoring studies do not show a significant reduction in blood pressure with HRT, suggesting loss of estrogen may not be the only factor involved in post-menopausal increases in BP. We hypothesize that it may be the post-menopausal lack of estrogen combined with the little change in testosterone levels that are the mechanisms by which blood pressure increases in older women. We are beginning experiments to test the hypothesis.