Physiology and Pharmacology

R. Douglas Wilkerson

Professor

Telephone: 419 383-4026 or 383-4182
FAX: 419 383-2871

e-mail: Doug.Wilkerson@utoledo.edu

Training

  • B.S., Pharmacy, 1967, University of North Carolina, Chapel Hill, NC
  • M.S., Pharmacology, 1969, Medical University of South Carolina, Charleston, SC
  • Ph.D., Pharmacology, 1972, Medical University of South Carolina, Charleston, SC

Appointments

  • Postdoctoral Fellow, Department of Pharmacology, Tulane University Medical School, New Orleans, LA, 1971-1973
  • Assistant Professor, Department of Pharmacology, University of South Alabama College of Medicine, Mobile, AL, 1973-1976
  • Associate Professor, Department of Pharmacology, University of South Alabama College of Medicine, Mobile, AL, 1976-1979
  • Associate Professor of Pharmacology and Therapeutics, Medical College of Ohio, 1979-1988
  • Professor of Pharmacology and Therapeutics, Medical College of Ohio, 1988- present
  • Associate Vice President for Research, Medical College of Ohio, 1991- present

  Research Interests:

Cardiovascular pharmacology, myocardial ischemia, cardiovascular effects of drugs.

Function of the heart and blood vessels is controlled by a number of influences including local factors (e.g., tissue metabolic activity), circulating hormones (e.g., epinephrine and angiotensin II) and activity of the autonomic nervous system. The major thrust of my research is the study of pharmacologic perturbations of these cardiovascular control processes. Most recently our emphasis has been on studies of pharmacologic modulation of autonomic tone to the cardiovascular system. Of specific interest, in this regard, has been studies of the effects of cocaine, a drug of abuse, on cardiovascular function. Cocaine exerts two primary pharmacologic effects: 1) it is a local anesthetic; and 2) it inhibits the major mechanism which terminates the action of norepinephrine, the chemical neurotransmitter released by nerves of the sympathetic division of the autonomic nervous system. Because these two actions generally elicit opposite effects on cardiac and vascular function, the cardiovascular actions of cocaine are very complex and poorly understood. My laboratory utilizes a number of in vitro and in vivo models to study the actions of cocaine on the heart and blood vessels. Some of the questions currently being addressed are: 1) Is the increase in blood pressure observed after administration of cocaine the result of an action on peripheral neurons, or is cocaine-induced central nervous system stimulation involved?; 2) What is the role of adrenal medullary epinephrine release in the cardiovascular actions of cocaine?; 3) Does cocaine modify baroreceptor function?; 4) Does cocaine interfere with autoregulation of coronary vascular function?; 5) Do other drugs beneficially or adversely modify the cardiovascular actions of cocaine?

Representative Publications

  • Foy, R.A., Myles, J.L., and Wilkerson, R.D. (1991): Contraction of bovine coronary vascular smooth muscle induced by cocaine is not mediated by norepinephrine. Life Sciences 49:299-308.
  • Temesy-Armos, P.N., Fraker, T.D., Brewer, P.S., and Wilkerson, R.D. (1992): The effects of cocaine on cardiac electrophysiology in conscious, unsedated dogs. J. Cardiovasc. Pharmacol. 19:883-891.
  • Foy, R.A., Myles, J.L., and Wilkerson, R.D. (1992): Characterization of 5-HT receptors in bovine coronary arteries. J. Pharmacol. and Exp. Therap. 261:601-606.
  • Chen, B.X., Myles, J.L., and Wilkerson, R.D. (1995): Role of the sympathoadrenal axis in the cardiovascular response to cocaine in conscious unrestrained rats. J. Cardiovasc. Pharmacol. 25:817-822.
  • Fraker, T.D., Temesy-Armos, P.N., Brewster, P.S., and Wilkerson, R.D. (1995): Interaction of propranolol, verapamil, and nifedipine on the myocardial depressant effect of cocaine. J. Cardiovasc. Pharmacol. 25:579- 586.
Last Updated: 3/22/15