β-Adrenoceptors in the medial amygdaloid nucleus modulate the tachycardiac response to restraint stress in rats

Abstract

In the present study, we investigated the involvement of β-adrenoceptors in the medial amygdaloid nucleus (MeA) in cardiovascular responses evoked in rats submitted to an acute restraint stress. We first pretreated Wistar rats with the nonselective β-adrenoceptor antagonist propranolol microinjected bilaterally into the MeA (10, 15, and 20nmol/100nL) 10min before exposure to acute restraint. The pretreatment with propranolol did not affect the blood pressure (BP) increase evoked by restraint. However, it increased the tachycardiac response caused by acute restraint when animals were pretreated with a dose of 15nmol, without a significant effect on the BP response. This result indicates that β-adrenoceptors in the MeA have an inhibitory influence on restraint-evoked heart rate (HR) changes.Pretreatment with the selective β2-adrenoceptor antagonist ICI 118,551 (10, 15, and 20nmol/100nL) significantly increased the restraint-evoked tachycardiac response after doses of 15 and 20nmol, an effect that was similar to that observed after the pretreatment with propranolol at a dose of 15nmol, without a significant effect on the BP response. Pretreatment of the MeA with the selective β1-adrenoceptor antagonist CGP 20712 (10, 15, and 20nmol/100nL) caused an opposite effect on the HR response, and a significant decrease in the restraint-evoked tachycardia was observed only after the dose of 20nmol, without a significant effect on the BP response. Because propranolol is an equipotent antagonist of both β1 and β2-adrenoceptors, and opposite effects were observed after the treatment with the higher doses of the selective antagonists ICI 118,551 and CGP 20712, the narrow window in the dose–response to propranolol could be explained by a functional antagonism resulting from the simultaneous inhibition of β1 and β2-adrenoceptors by the treatment with propranolol.The present results suggest that β2-adrenoceptors have an inhibitory influence on the restraint-evoked tachycardiac response, whereas β1-adrenoceptors have a facilitatory influence on the restraint-evoked tachycardiac response.