John C. Hancock, Ph.D.
Professor Emeritus

Research Interests:

My principal research interest is to evaluate neural regulation of cardiovascular function in normal conditions and during the development of hypertension. Studies are conducted on normotensive rats, rats with a genetic form of hypertension (spontaneously hypertensive rats; SHR), normotensive rats that have been made hypertensive and SHR that are kept from becoming hypertensive. Both the genetic model and humans with hypertension have increases in sympathetic nerve activity and the heightened nerve activity is thought to be the initiating cause of hypertension. The focus my laboratory is to determine the cause of the increase in sympathetic nerve activity. We are currently conducting functional studies in which we correlate changes in sympathetic nerve activity with the changes in cardiovascular hemodynamics caused by peptide neurotransmitter stimulation of postganglionic sympathetic neurons. For these studies, we compare the electrical patterns of sympathetic nerve firing in anesthetized normotensive and hypertensive rats by computer assisted analysis of frequency patterns. We are also investigating control of sympathetic nerve function in normotensive and hypertensive animals at the cellular level using intracellular microelectrode techniques,autoradiography to determine receptor number and mRNA using polymerase chain reaction to determine peptide receptor mRNA.

Our laboratory is also conducting studies on the response of individual neurons in intrinsic cardiac ganglia to tachykinins and other sensory neurotransmittes using microelectrode techniques. Results from these studies are correlated with the effects of the sensory neurotransmitters on anesthetized animals to determine the functional correlate of that information in the whole animal. This information provides the foundation for understanding the integrated neural responses of the cardiac nervous system to such stresses as myocardial ischemia and heart failure.

My research is supported in part by the National Institutes of Health, HL54633 (Donald Hoover, PI)

Selected Publications:

Hancock, J.C. and Lindsay, G.W.: Pressor and tachycardic responses to substance P in anesthetized rats. Peptides 16:1439-1445, 1995

Tompkins J.D., Hoover, D.B., and Hancock, J.C.: Substance P evokes bradycardia by stimulation of postganglionic cholinergic neurons. Peptides 20:623-628, 1999.

Hancock J.C. and Lindsay, G.W.: Enhancement of ganglion responses to substance P in spontaneously hypertensive rats. Peptides 21:535-541, 2000.

Schoborg, R.V., Hoover, D.B., Tompkins, J.D., and Hancock, J.C.: Increased ganglionic responses to substance P in hypertensive rats is due to up-regulation of NK1 receptors. American Journal of Physiology (Regulatory Integrative Comp. Physiol) 279: R1685-R1694, 2000

Zhang, L, Tompkins, J.D., Hancock, J.C., and Hoover, D.B.: Substance P modulates nicotinic responses of intriacardiac neurons to acetylcholine in the guinea pig. American J. Physiology Regulatory Integrative Comp. Physio 281, R1792-R1800, 2001.

Tompkins, J.D. and Hancock, J.C.: Electrophysiological effects of tachykinin agonists on sympathetic ganglia of spontaneously hypertensive rats. Autonomic Neuroscience: Basic and Clinical , 97: 26-34, 2002.

Morales, M.A., Hancock, J.C., and Hoover, D.B.: Neurochemical heterogeneity in sympathetic ganglia and its implications for cardiovascular regulations. In: N.J.

Dun, B.H., Machado and P.M. and P.M. Pilowsky (Eds.) Neural Mechanisms of Cardiovascular Regulation. Kluwer Academic Publishers, (Pages 303-333), 2004

Chang, Y., L.J. Lawson, Hancock, J.C., and Hoover, D.B.: Pituitary adenylate cyclase-activating polypeptide: localization and differential influence on isolated hearts from rats and guinea pigs Regulatory Peptides, 129/1-3, 139-146, 2005.

Zhang, L., Hancock, J.C., and Hoover, D.B.: Tachykinin agonists modulate cholinergic neurotransmission at guinea pig intracardiac ganglia. J. Pharmacol Sci. (In revision).