Pharmacology 1000: Fundamentals of Pharmacology Pharmacology 1010: Pharmacology I
Pharmacology 1020: Pharmacology II
Pharmacology 2010: Cardiovascular Pharmacology
Pharmacology 3010: Career Pathways in Pharmacology
Phone: (914) 594-4138/4131
Department of Pharmacology
Basic Science Building, Rm. 547/508
15 Dana Road
Valhalla, NY 10595
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.