email: steven.bealer@utah.edu

Professor of Pharmacology and Toxicology Neurobiology of Disease

B.S. 1971, University of Wyoming; Ph.D. 1976, University of Wyoming.

RESEARCH:

Ongoing studies are directed at understanding mechanisms by which seizure disorders alter cardiac function, that results in increased risk of sudden cardiac death. We are using rodent models of status epilepticus and temporal lobe epilepsy to investigate the contribution of the sympathetic nervous system in enhanced susceptibility to lethal ventricular arrhythmias characteristic of these seizure disorders.

Selected Publications

Bealer, S.L., Metcalf, C.S., and Heyborne, R. (2007) Increased dietary sodium alters Fos expression in the lamina terminalis during intravenous angiotensin II infusion. Experimental Neurology, 204:299-306.

Bealer, S.L., Lipschitz, D.L., Ramoz, G., and Crowley, R.W. (2006) Oxytocin receptor binding in magnocellular nuclei during gestation in rats. American Journal of Physiology: Reg., Int., and Comp. Physiol., 291:R53-R58.

Bealer, S.L. (2005) Increased dietary sodium inhibits baroreflex-induced bradycardia during acute sodium loading. American Journal of Physiology (Regulatory, Integrative and Comparative Physiology), 288:R1211-R1219.

Bealer, S.L., and Metcalf, C.S. (2005) Increased dietary sodium enhances activation of neurons in the medullary cardiovascular pathway during acute sodium loading in the rat. Autonomic Neuroscience, 117:33-40.

Lipschitz, D.L., Crowley, R.W., and Bealer, S.L. (2004) Differential sensitivity of intranuclear and systemic oxytocin release to central noradrenergic receptor stimulation during mid- and late gestation in rats. American Journal of Physiology (Endocrinology and Metabolism), 287:E523-E528.

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