Simon O R, Basuray B N, West W L, Copeland R
Neuropharmacology. 1985 Jul;24(7):665-75. doi: 10.1016/0028-3908(85)90110-8.
Cats, anaesthetized with alpha-chloralose, were used to investigate an interaction between the baroreceptor reflex and stimulation of the anterior hypothalamus (AH). In these cats, stimulation of the anterior hypothalamus gave autonomic responses that characterize the defense reaction. Stimulation of the anterior hypothalamus also interacted with the baroreceptor reflex without altering the effectiveness of the vasodepressor component of the reflex (induced by stimulation of the aortic nerves). However, in spinal cats the bradycardia component (induced by angiotensin at 0.097 nmol/kg pe min, i.v.) was inhibited by stimulation of the anterior hypothalamus and the inhibition was augmented by pretreatment with phentolamine (17.7 nmol) in the nucleus tractus solitarius (NTS). Pretreatment with phentolamine (17.7 nmol) in the nucleus tractus solitarius also reduced the sensitivity of the bradycardia component of the reflex and attenuated (3 and 6 nmol) the induced inhibition of the bradycardia induced by stimulation of the anterior hypothalamus. This attenuation induced by NE was abolished by pretreatment with phentolamine (17.7 nmol), but not by pretreatment with sotalol (16 nmol) or haloperidol (12 nmol) in the nucleus tractus solitarius. Additionally, NE was released from the nucleus tractus solitarius during activation of the baroreceptor and during stimulation of the anterior hypothalamus in cats with intact baroreceptor nerves, but not in baroreceptor-denervated cats. Moreover, the baroreceptor reflex attenuated the pressor response evoked by stimulation of the anterior hypothalamus, and also caused the release of NE from the anterior hypothalamus. At this site, injection of NE (3 and 6 nmol) attenuated the pressor response evoked by stimulation of the anterior hypothalamus and this attenuation was abolished by pretreatment with phentolamine (17.7 nmol), but not by pretreatment with sotalol (16 nmol) or haloperidol (12 nmol) in the anterior hypothalamus. It is concluded that NE participates at the nucleus tractus solitarius and the anterior hypothalamus as an attenuator in the interaction between the baroreflex and stimulation of nerve fibers in the anterior hypothalamus that mediate the defense reaction.
用α-氯醛糖麻醉的猫来研究压力感受器反射与刺激下丘脑前部(AH)之间的相互作用。在这些猫中,刺激下丘脑前部会产生自主反应,这些反应是防御反应的特征。刺激下丘脑前部还会与压力感受器反射相互作用,但不会改变反射的血管减压成分(由刺激主动脉神经诱导)的有效性。然而,在脊髓猫中,下丘脑前部的刺激会抑制(静脉注射0.097 nmol/kg每分钟的血管紧张素诱导的)心动过缓成分,并且在孤束核(NTS)中用酚妥拉明(17.7 nmol)预处理会增强这种抑制作用。在孤束核中用酚妥拉明(17.7 nmol)预处理也会降低反射的心动过缓成分的敏感性,并减弱(3和6 nmol)下丘脑前部刺激诱导的心动过缓抑制。这种由去甲肾上腺素(NE)诱导的减弱作用在孤束核中用酚妥拉明(17.7 nmol)预处理后被消除,但用索他洛尔(16 nmol)或氟哌啶醇(12 nmol)预处理则不能消除。此外,在具有完整压力感受器神经的猫中,在压力感受器激活期间以及刺激下丘脑前部期间,NE从孤束核释放,但在压力感受器去神经的猫中则不会。此外,压力感受器反射会减弱下丘脑前部刺激诱发的升压反应,并且还会导致NE从下丘脑前部释放。在这个部位,注射NE(3和6 nmol)会减弱下丘脑前部刺激诱发的升压反应,并且这种减弱作用在丘脑前部下用酚妥拉明(17.7 nmol)预处理后被消除,但用索他洛尔(16 nmol)或氟哌啶醇(12 nmol)预处理则不能消除。得出的结论是,NE在孤束核和下丘脑前部作为一种减弱剂参与压力反射与介导防御反应的下丘脑前部神经纤维刺激之间的相互作用。