Division of Nephrology and Hypertension
Department of Medicine
Georgetown University Medical Center
6 PHC3800 Reservoir Road, NW
Washington, DC 20057
Phone: 202 784-3006
Fax: 240 255-3046
Mechanisms of vascular dysfunction in hypertensive disorders of pregnancy and in menopause
Our major focus is to elucidate mechanisms of normal gestational vasodilation in human and animal pregnancy and of enhanced vasoconstriction and endothelial dysfunction in preeclamptic women. These studies focus on in vitro functional and molecular study of small resistance arteries. We hypothesize that enhanced angiotensin II (ang II) signaling leads to oxidative stress, selectively augmenting vasoconstrictor response and impairing endothelium-dependent relaxation. This construct, derived from our recent work in several animal models of low-dose ang II infusion is also being applied in pilot studies of menopausal women, as estrogen appears to inhibit ang II induced oxidative stress by several distinct mechanisms. These protocols along with others focused on diagnosis and treatment of hypertension in pregnant women are facilitated by my clinical expertise in hypertensive and renal disorders in pregnancy, leading to my role as a medical consultant to obstetricians and maternal-fetal medicine specialists.
- Pascoal IF, Lindheimer MD, Nalbantian-Brandt C, Umans JG: Preeclampsia selectively impairs endothelium dependent relaxation and leads to oscillatory activity in small omental arteries. J Clin Invest 101:464-470, 1998.
- Umans JG, Lindheimer MD, Hack B, Davidson-Garcia CA: Connexin expression is not altered in omental resistance vessels from women with preeclampsia. Hypertens Pregnancy 20:119-24, 2001.
- Wylam ME, Metkus AP, Umans JG: Nitric oxide dependent and independent effects of in vitro incubation or endotoxin on vascular reactivity in rat aorta, Life Sci 69:455-67, 2001.
- Umans JG, Lindheimer MD: Antihypertensive therapy in pregnancy. Curr Hypertens Rep 3:392-9, 2001
- Wang D, Borrego-Conde LJ, Falck JR, Sharma KK, Wilcox CS, Umans JG: Contributions of NO, EDHF and EETs to endothelium-dependent relaxation in renal afferent arterioles. Kidney Int, 2003, in press.