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Repeated restraint stress-induced increase in baroreceptor reflex sensitivity: role of corticotropin-releasing factor
L H Conti1, M H Shannon, J D Murry
1Department of Pharmacology, University of California, San Diego, La Jolla, CA 92093, USA. Lconti@ucsd.edu
Abstract:
The effect of central administration of a corticotropin-releasing factor antagonist on repeated restraint stress-induced changes in the baroreceptor reflex response to phenylephrine was examined in male Wistar-Kyoto rats. Rats were instrumented with intracerebroventricular guide cannula and femoral arterial and venous catheters. On each of 5 consecutive days, two groups received either a central infusion of saline or an infusion of the corticotropin-releasing factor antagonist, astressin. One saline- and one astressin-treated group experienced 20 min of restraint stress 10 min after each infusion. The other saline- and astressin-treated groups served as non-stressed controls. Twenty-four hours later, each rat received 3 doses of phenylephrine which produced equivalent increases in mean arterial pressure in each of the 4 treatment groups. Reflex bradycardia was significantly greater in the saline-treated/repeated restraint group than in the saline-treated/no restraint group. This effect of repeated restraint on the baroreceptor reflex was attenuated by administration of astressin prior to each session of restraint. A single 20 min session of restraint stress failed to alter baroreceptor reflex sensitivity. However, repeated central infusions of exogenous CRF failed to alter BRR sensitivity. In a separate experiment, astressin failed to attenuate the increases in mean arterial pressure and heart rate which occurred during each session of restraint stress and, in fact, diminished habituation of the blood pressure response in the last session. The results suggest that repeated stress increases thesensitivity of the baroreceptor reflex and that corticotropin-releasing factor has a role in this stress-induced change.
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