The role of peripheral beta 2-adrenoceptors in the cardiovascular response to acute stress was examined in adult Wistar-Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and the first generation (F1) cross of WKY and SHR. In experiment 1, WKY, SHR, and F1 were exposed to two stressors, transfer to a novel chamber and foot shock, after treatment with either vehicle or the beta 2-adrenoceptor antagonist ICI 118,551. SHR and F1 treated with ICI 118,551 had greater pressor responses to the stress of transfer and to foot shock than vehicle-treated controls. In contrast, the cardiovascular response of WKY to the stressors was not affected by beta 2-adrenoceptor antagonism. These results suggest that beta 2-adrenoceptors are activated during acute stress in SHR and F1 to reduce large pressor episodes, but this mechanism is not utilized in WKY. A second study examined the effects of beta 2-adrenoceptor antagonism on resting arterial pressure. Resting heart rate and pressure were not significantly different between vehicle- and ICI 118,551-treated animals. However, the pressor response to the stressors was greater in ICI 118,551- than vehicle-treated F1, but the tachycardia was equivalent for both groups. These results demonstrate that beta 2-adrenoceptor antagonism can selectively enhance pressor responses to stress without affecting heart rate responses. Together, these results suggest that activation of beta 2-adrenoceptors during acute stress may blunt large pressor responses in SHR and F1, which may be related to the exaggerated sympathoadrenal response to stress that is characteristic of SHR.
- Copyright © 1990 the American Physiological Society