Christine Baylis, PhD
Christine Baylis, PhD
Division of Nephrology, Hypertension & Renal Transplantation
Professor of Physiology/Medicine
Director of the Hypertension Center
1600 SW Archer Road
Room M556, MSB
PO Box 100274
Gainesville, FL 32610-0274
TEL: (352) 392-7869
|PhD||Leeds University||Renal Physiology|
|Postdoctoral Fellow||UC San Francisco||Nephrology|
|Postdoctoral Fellow||Brigham and Womens Hospital/Harvard Medical School||Nephrology|
Dr. Baylis’ renal physiology specific interest areas include: renal hemodynamics; blood pressure control; kidney in pregnancy; aging kidney; sexual dimorphism in kidney function and blood pressure control; nitric oxide in renal physiology and disease; progression of kidney disease; and vascular endothelial function. Her research centers on the kidney and blood pressure control with specific interests in several areas.
One area relates to maternal adaptations during normal and compromised pregnancy and the current research is devoted to understanding the renal mechanisms of the normal maternal plasma volume expansion which is so important in an optimal outcome for the developing fetus. The Baylis lab has amassed considerable evidence that the normal maternal volume expansion requires a localized increase in the activity of phosphodiesterase-5 (PDE5), in the inner medulla of the kidney. This prevents the normal natriuretic influences that work through cGMP (nitric oxide, NO and atrial natriuretic peptide) from acting and allows the activated sodium retaining influences (angiotensin II and aldosterone) to dominate renal sodium handling, leading to continual renal sodium retention throughout pregnancy.
A second major interest of Dr. Baylis is in the role of NO deficiency in the pathogenesis of chronic kidney disease (CKD) and associated cardiovascular disease. One active area of investigation is on how the intra-renal NO synthases influence progression of CKD and also the way that the endogenous NO synthase inhibitor, asymmetric dimethylarginine (ADMA) is regulated and contributes to endothelial dysfunction, cardiovascular injury and progression of CKD. It is now clear that systemic and intra-renal NO deficiency are both a cause and a consequence of CKD, contributing importantly to progression of the kidney damage and to the associated cardiovascular disease. In related studies, Dr. Baylis is also investigating how metabolism and transport of the NO synthase substrate L-arginine changes in CKD and may contribute to NO deficiency. A new area is investigating the impact of exercise on the kidney and specifically on the renal NO and antioxidant systems. Despite the many beneficial metabolic and cardiovascular effects of exercise, it is also found that in some rats, exercise renders the kidney susceptible to exacerbation experimentally induced acute renal failure.
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