Kirby R F, Johnson A K
Department of Psychology, University of Iowa, Iowa City 52242.
Am J Physiol. 1990 Mar;258(3 Pt 2):H683-8. doi: 10.1152/ajpheart.1990.258.3.H683.
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.
在成年Wistar-Kyoto大鼠(WKY)、自发性高血压大鼠(SHR)以及WKY和SHR的第一代杂交后代(F1)中,研究了外周β2-肾上腺素能受体在急性应激心血管反应中的作用。在实验1中,WKY、SHR和F1在用溶剂或β2-肾上腺素能受体拮抗剂ICI 118,551处理后,暴露于两种应激源,即转移至新的实验箱和足部电击。用ICI 118,551处理的SHR和F1对转移应激和足部电击的升压反应比用溶剂处理的对照组更大。相比之下,WKY对应激源的心血管反应不受β2-肾上腺素能受体拮抗作用的影响。这些结果表明,在急性应激期间,SHR和F1中的β2-肾上腺素能受体被激活以减少大的升压发作,但WKY未利用这种机制。第二项研究考察了β2-肾上腺素能受体拮抗作用对静息动脉压的影响。用溶剂和ICI 118,551处理的动物之间的静息心率和血压无显著差异。然而,ICI 118,551处理的F1对应激源的升压反应比用溶剂处理的更大,但两组的心动过速情况相当。这些结果表明,β2-肾上腺素能受体拮抗作用可选择性增强对应激的升压反应而不影响心率反应。总之,这些结果表明,急性应激期间β2-肾上腺素能受体的激活可能减弱SHR和F1中的大升压反应,这可能与SHR特有的对应激过度的交感肾上腺反应有关。