NYMC > Faculty > Directory > By Name > Stier, Charles

Charles T. Stier, Ph.D.

Associate Professor of Pharmacology
Director, M.S. Program in Pharmacology

Course Director:

Pharmacology 1000:  Fundamentals of Pharmacology Pharmacology 1010:  Pharmacology I
Pharmacology 1020:  Pharmacology II
Pharmacology 2010:  Cardiovascular Pharmacology
Pharmacology 3010:  Career Pathways in Pharmacology

E-mail:  charles_stier@nymc.edu

Phone: (914) 594-4138/4131

Address:
Department of Pharmacology
Basic Science Building, Rm. 547/508
15 Dana Road
Valhalla, NY  10595

Research Interests:

Dr. Stier’s research activities over the past two decades have been supported by grants from the National Institutes of Health, the American Heart Association, and the pharmaceutical industry. He has published over 80 papers on various vascular and renal mechanisms relevant to the control of blood pressure in normotensive and hypertensive settings. Dr. Stier has gained national and international recognition for establishing that pharmacological interventions that interfere with the activity of the renin-angiotensin-aldosterone system protect against development of end organ damage in stroke prone spontaneously hypertensive rats, via a mechanism that does not depend on lowering of blood pressure.  Dr. Stier’s laboratory has over 20 years of experience in the measurement of blood pressure using radiotelemetry techniques.  Recent research studies in Dr. Stier’s laboratory have focused on the role of lipid mediators such as EETs and 20-HETE on target organ damage not only in stroke-prone hypertensive rats but in other models of hypertension as well.

Current Research Interests:

It is well-known that high-salt intake can be a causative factor in blood pressure elevation. However, little is known about how high salt-intake can sensitize to end-organ damage (stroke, myocardial infarction and renal dysfunction). Our previous data, indicate that high blood pressure alone may not be sufficient to provoke vascular injury in our stroke-prone spontaneously hypertensive rat (SHRSP) model of end-organ damage. Recent evidence had linked epoxyeicosatrienoic acids (EETs) to the prevention of end-organ damage and high-salt intake to the release of EETs. Our recently published studies and preliminary data indicate a strong connection between EETs and prevention of salt-sensitive end-organ damage in SHRSP. These studies will provide information relevant to the development of clinical therapeutic interventions to combat end-organ damage beyond that of lowering blood pressure.

The metabolic syndrome is a condition characterized by elevated blood pressure, obesity, hypertriglyceridemia, and insulin insensitivity. The metabolic syndrome has also been referred to as syndrome X.  Patients with the metabolic syndrome thus display multiple derangements which feature not only hypertension but also diabetes and hyperlipoproteinemia. One of the obstacles to the study of the metabolic syndrome has been the availability of an animal model which possesses all the phenotypic changes that are present clinically. One model is the obese spontaneously hypertensive rat (SHROB) which was original developed by Dr. Koletsky. These animals are now commercially available from Charles River Laboratories. In planned studies, we will more fully characterize the chronological development of the metabolic syndrome phenotype in these rats. Our goal is to establish this animal model for future studies to investigate to agents such as niacin, and niacin-like compounds, which have a profile of activities that should result in prevention or reversal of the metabolic syndrome.

Selected Publications:

  1. Rocha, R., P.N Chander, K. Khanna, A. Zuckerman and C.T. Stier, Jr.  Mineralocorticoid blockade reduces vascular injury in stroke-prone hypertensive rats.  Hypertension.  31:451-458, 1998.
  2. Rocha, R., P.N. Chander, A. Zuckerman and C.T. Stier, Jr.  Role of aldosterone in renal vascular injury in stroke-prone hypertensive rats.  Hypertension.  33:232-237, 1999.
  3. Stier, C.T., Jr., P.N. Chander and R. Rocha.  Aldosterone as a mediator of cardiovascular injury.  Cardiology in Review.  10(2):97-106, 2002.
  4. Chander, P.N., R. Rocha, J. Ranaudo, G. Singh, A. Zuckerman and C.T. Stier, Jr.  Aldosterone plays a pivotal role in the pathogenesis of thrombotic microangiopathy in SHRSP.  Journal of the American Society of Nephrology.  14(8):1990-1997, 2003.
  5. Li, J., M.A. Carroll, P.N. Chander, J.R. Falck, B. Sangras and C.T. Stier, Jr.  Soluble epoxide hydrolase inhibitor, AUDA, prevents early salt-sensitive hypertension.  Frontiers in Bioscience.  13:3480-3487, 2008.
  6. Chun, T-Y., P.N. Chander, J-W. Kim, J.H. Pratt and C.T. Stier, Jr.  Aldosterone, but not angiotensin II, increases profibrotic factors in kidney of adrenalectomized stroke-prone spontaneously hypertensive rats.  Am J Physiol Endocrinol Metab.  295(2):E305-E312, 2008.
  7. Sabban, E.L., N. Schilt, L.I. Serova, S.N. Masineni and C.T. Stier, Jr.  Kinetics and persistence of cardiovascular and locomotor effects of immobilization stress and influence of ACTH treatment.  Neuroendocrinology.  89(1):98-108, 2009.
  8. Liclican, E.L., A.B. Doumad, J. Wang, J. Li, J.R. Falck, C.T. Stier, Jr. and M.A. Carroll.  Inhibition of the adenosine 2A receptor-epoxyeicosatrienoic acid pathway renders Dahl salt-resistant rats hypertensive.  Hypertension.  54(6):1284-1290, 2009.
  9. Chen, C.C., P.L. Pedraza, S. Hao C.T. Stier and N.R. Ferreri.  TNFR1 deficient mice display altered blood pressure and renal responses to Ang II infusion.  American Journal of Physiology – Renal Physiology.  299(5):F1141-F1150, 2010.
  10. Jiang, H., J. Quilley, A.B. Doumad, A.G. Zhu, J.R. Falck, B.D. Hammock, C.T. Stier and M.A. Carroll.  Increases in plasma trans-EETs and blood pressure reduction in spontaneously hypertensive rats.  American Journal of Physiology – Heart and Circulatory Physiology.  300(6):F1990-F1196, 2011.
  11. Battula, S., S. Hao, P.L. Pedraza, C.T. Stier and N.R. Ferreri.  Tumor necrosis factor-alpha induces renal cyclooxygenase-2 expression in response to hypercalcemia in vivo.  Prostaglandins and Other Lipid Mediators.  99(1-2): 45-50, 2012.
  12. Stier, C.T., Jr.  Vascular effects of high-salt intake.  J Hypertens.  31(3):472-473, 2013.
  13. Li, J., C.T. Stier, P.N. Chander, V.L. Manthati, J.R. Falck and M.A. Carroll.  Pharmacological manipulation of arachidonic acid-epoxygenase results in divergent effects on renal damage.  Accepted for publication in Frontiers in Pharmacology, 2014.
  14. Carroll MA, Kang YJ, Chander PN, Stier CT Jr.  Azilsartan, an ARB, is associated with increased circulating angiotensin-(1-7) levels and reduced renovascular 20-HETE levels.  Accepted for publication in the American Journal of Hypertension, 2014.

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