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Faculty Detail    
Name DAVID POLLOCK
  
Campus Address KAUL 802B Zip 0006
Phone  (205) 975-7526
E-mail  davidpollock@uabmc.edu
Other websites
     

Education
Undergraduate  University of Evansville    1978  B.S. 
Graduate  University of Cincinnati    1983  Ph.D. 


Faculty Appointment(s)
Appointment Type Department Division Rank
Primary  Med - Nephrology  Med - Nephrology Professor
Center  Comprehensive Cardiovascular Ctr  Comprehensive Cardiovascular Ctr Professor
Center  Comprehensive Diabetes Center  Comprehensive Diabetes Center Professor
Center  Ctr for Clinical & Translational Sci  Ctr for Clinical & Translational Sci Professor
Center  Ctr for Free Radical Bio  Ctr for Free Radical Bio Professor
Center  Nephrology Research & Training Center  Nephrology Research & Training Center Professor
Center  Nutrition Sciences Research  Nutrition Obesity Res Ctr (NORC) Professor

Graduate Biomedical Sciences Affiliations
Pathobiology and Molecular Medicine 

Biographical Sketch 
David Pollock is Professor in the Division of Nephrology Department of Medicine at the University of Alabama at Birmingham. He serves as Director of the Cardio-Renal Physiology and Medicine section, a translational research program supported jointly by the Division of Cardiovascular Disease and Division of Nephrology. Pollock earned his Ph.D. degree in Physiology from the University of Cincinnati in 1983 with Robert Banks as his advisor. His thesis project comprised some of the first papers ever published on the renal actions of atrial natriuretic factor. He then completed a post-doctoral fellowship at the University of North Carolina at Chapel Hill under the direction of William Arendshorst in the world-famous micropuncture lab run by Carl W. Gottschalk. He conducted a series studies related to mechanisms of autoregulation of renal blood flow and tubuloglomerular feedback. He then spent two years as a Senior Scientist at the Institute for Circadian Physiology at Harvard University in Boston where he worked on a NASA supported project studying fluid volume regulation in a ground-based model of weightlessness. In 1989, he took a position in the Drug Discovery division of Abbott Laboratories in Chicago. While at Abbott, he worked on several projects including atrial peptide analogs, angiotensin receptor antagonists, and endothelin receptor antagonists. Most of his work focused on proof of concept studies in various animal models of hypertension and renal disease. In 1995, Pollock moved back to academia and accepted a faculty position at the Medical College of Georgia (now known as Georgia Regents University) where he served as a faculty member in the Vascular Biology Center and eventually led the establishment of the Experimental Medicine section in the Department of Medicine. In January 2014, Pollock moved to his current position at the University of Alabama at Birmingham where he is leading the development of a translational research group focusing on renal and cardiovascular physiology. Pollock’s research has been continuously supported by a series of National Institutes of Health and American Heart Association (AHA) grants including an AHA Established Investigator Award from 2000-2005. He currently serves as Principal investigator on a Heart Lung and Blood Institute (NHLBI) Program Project Grant (PPG) focusing integrated control of renal water and electrolyte handling. This work is a collaborative effort with UAB faculty, Jennifer Pollock and Edward Inscho as well as Donald Kohan at the University of Utah and James Stockand at the University of Texas at San Antonio. Pollock also serves as Deputy Director and Project Leader on another NHLBI-funded PPG focusing on stress and obesity in hypertension risk. Since August of 2013, Pollock has been Co-PI of a Center Grant (U01) investigating the role of endothelin in sickle cell nephropathy in both animal models and humans. He has also held a series of investigator-initiated grants from companies including Abbott Labs, Takeda and Astra-Zeneca Pharmaceuticals and has served as a scientific advisor for Abbott, Gilead, Speedel, and Astra-Zeneca. He has served on many NIH and AHA scientific peer review panels including the AHA National Cardio-Renal study section where he served as chair and the NIH F10A panel on organ system pathophysiology reviewing individual training grants since 2005. Pollock has authored more than 180 peer-reviewed papers along with over 40 invited reviews and commentaries and 11 book chapters including one as editor. Pollock recently completed a 6 year term as Associate Editor for the American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. He is currently Editor-in-Chief of Comprehensive Physiology. Pollock has also served as Associate Editor of Vascular Pharmacology as well as several other guest editorships. He currently serves on the editorial boards of Physiological Reviews, The American Journal of Physiology: Heart and Circulatory Physiology, Hypertension, and Nitric Oxide: Biology and Chemistry. Pollock has been active in a wide range of national and international organizations. He recently served as the 87th President of the American Physiological Society (APS). He is currently serving as Chair of the APS Conference Committee and has organized several conferences with APS as well as a FASEB Summer Conference, the International Conference on Endothelin, and a Forefronts Conference with the International Society of Nephrology. He serves as a founding member of the International Advisory Board for the bi-annual conferences on endothelin. Pollock has also served on numerous committees with APS and AHA. Pollock has received a number of honors and awards including the Louis K Dahl Award for hypertension research from the AHA in 2013 and the Ernest Starling Award Lecturer in 2016.



Research/Clinical Interest
Title
Hypertension and Renal Disease
Description
Pollock’s research focuses on elucidating control mechanisms of sodium excretion and the role of the kidney in blood pressure regulation. His long-standing interest in natriuretic factors has led to his active involvement in deciphering the actions of endothelin, primarily within the kidney but also in vascular and nervous systems. His research has helped to elucidate the opposing actions of endothelin A versus endothelin B receptors in both renal vasculature and the tubular system. Recent studies from his lab have suggested that defects in the endothelin B receptor system contribute to salt-sensitivity in hypertension. More recently, his research has included collaborators conducting human studies that address these same mechanisms. His work also includes the role of endothelin in glomerular injury where his lab has conducted important proof of concept studies providing evidence that endothelin contributes directly to diabetic glomerular dysfunction and that ETA receptor antagonists exert therapeutic benefit as recently shown in clinical trials. This work has extended beyond diabetes and now includes sickle nephropathy, a problem of rising incidence in subjects with sickle cell disease. Much of his most recent work has been to uncover circadian control of renal excretory function including the discovery that high salt diet impacts clock gene expression in the kidney.

Keywords
hypertension, diabetes, sickle cell, hemodynamics, endothelin, nitric oxide, kidney, sodium