Central beta-adrenoceptors mediate phasic and sustained components of hemodynamic responses to acute behavioral stress

Abstract

Startle elicits a pattern of cardiovascular responses that is consistent within individual rats but varies between rats. We examined the hypothesis that central beta-adrenoceptors mediate differences in the hemodynamic responses to stress. Conscious rats exposed to cold water (1 cm deep, 1 min) had an initial phasic (startle) response (first 5 s) that varied considerably between rats. We designated those rats with an initial increase in cardiac output (CO) and systemic vascular resistance (SVR) as mixed responders while those with only an increase in SVR were vascular responders. Propranolol pretreatment (3 microg, icv) made the phasic changes in CO more negative, whereas isoproterenol (3 microg) made the CO response more positive in mixed responders and attenuated the increases in arterial pressure and SVR in vascular responders. Metoprolol (30 microg, icv) depressed the change in CO due to startle in mixed responders by decreasing heart rate. ICI 188,551 (25 microg, icv) did not alter the responses to startle but depressed the heart rate and CO responses and enhanced the pressor and SVR responses to sustained stress (1 min exposure to cold water). The results suggest that startle elicits hemodynamic responses that are primarily dependent on beta1-adrenoceptors but responses to sustained stress are dependent on beta2-adrenoceptors in the CNS.