AJP - Regulatory, Integrative and Comparative Physiology, Vol 258, Issue 3 596-R601, Copyright © 1990 by American Physiological Society
Central nervous system cardiovascular actions of CRF in sinoaortic-denervated rats
J. M. Overton, G. Davis-Gorman and L. A. Fisher
Department of Pharmacology, University of Arizona College of Medicine, Tucson 85724.
Studies were performed in unrestrained conscious Sprague-Dawley rats to
examine the central nervous system (CNS) mechanism by which
corticotropin-releasing factor (CRF) produces simultaneous elevations of
arterial pressure and heart rate. To test the hypothesis that CRF inhibits
ongoing impulse transmission through and/or transmitter release from the
CNS terminations of baroreceptor afferents, the cardiovascular effects of
intracerebroventricular administration of CRF were compared in rats
subjected to prior sham surgery (Sham) or sinoaortic denervation (SAD).
Resting levels of arterial pressure and heart rate were elevated after SAD.
In addition, SAD resulted in greater chronotropic sympathetic tone and
reduced chronotropic parasympathetic tone as assessed by intravenous
injections of atropine methyl nitrate and DL-propranolol.
Intracerebroventricular administration of CRF in both surgical groups
elicited significant increases in arterial pressure and heart rate,
although a tendency for reduced tachycardic responses after SAD was
apparent. Pretreatment with atropine or propranolol revealed that both the
parasympathetic and sympathetic nervous systems contribute to CRF-induced
heart rate responses in both surgical groups. These results suggest that
ongoing baroreceptor afferent transmission is not requisite for the
expression of CRF-induced cardiovascular changes. Thus it is unlikely that
CRF elevates arterial pressure and heart rate through an exclusive action
at the CNS terminations of baroreceptor sensory fibers.
