首页> 外文期刊>American Journal of Physiology >5-HT-mediated inhibition of cardiovagal baroreceptor reflex response during defense reaction in the rat.
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5-HT-mediated inhibition of cardiovagal baroreceptor reflex response during defense reaction in the rat.

机译:5-HT介导的大鼠防御反应过程中对心肌血管压力感受器反射反应的抑制。

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Previous studies showed that the cardiac response of the baroreceptor reflex (bradycardia) is inhibited during the defense reaction evoked by direct electrical or chemical stimulation of the periaqueductal gray (dPAG) in the rat. Whether central serotonin and nucleus tractus solitarius (NTS) serotonin(3) (5-HT(3)) receptors might participate in this inhibition was investigated in urethane-anesthetized and atenolol-pretreated rats. Our results showed that both electrical and chemical stimulation of the dPAG produced a drastic reduction of the cardiovagal component of the baroreceptor reflex triggered by either intravenous administration of phenylephrine or aortic nerve stimulation. This inhibitory effect of dPAG stimulation on the baroreflex bradycardia was not observed in rats that had been pretreated with p-chlorophenylalanine (300 mg/kg ip daily for 3 days) to inhibit serotonin synthesis. Subsequent 5-hydroxytryptophan administration (60 mg/kg ip), which was used to restore serotonin synthesis, allowed the inhibitory effect of dPAG stimulation on both aortic and phenylephrine-induced cardiac reflex responses to be recovered in p-chlorophenylalanine-pretreated rats. On the other hand, in nonpretreated rats, the inhibitory effect of dPAG stimulation on the cardiac baroreflex response could be markedly reduced by prior intra-NTS microinjection of granisetron, a 5-HT(3) receptor antagonist, or bicuculline, a GABA(A) receptor antagonist. These results show that serotonin plays a key role in the dPAG stimulation-induced inhibition of the cardiovagal baroreceptor reflex response. Moreover, they support the idea that 5-HT(3) and GABA(A) receptors in the NTS contribute downstream to the inhibition of the baroreflex response caused by dPAG stimulation.
机译:先前的研究表明,通过直接电刺激或化学刺激大鼠导水管周围灰色(dPAG)诱发的防御反应期间,压力感受器反射(心动过缓)的心脏反应受到抑制。在氨基甲酸乙酯麻醉的和阿替洛尔预处理的大鼠中研究了中央5-羟色胺和孤束核(NTS)5-羟色胺(3)(5-HT(3))受体是否可能参与这种抑制作用。我们的研究结果表明,dPAG的电刺激和化学刺激均会导致静脉注射去氧肾上腺素或主动脉神经刺激引起的压力感受器反射的心肌迷走神经成分急剧减少。在用对氯苯丙氨酸(每天300 mg / kg ip每天3天)预处理以抑制5-羟色胺合成的大鼠中未观察到dPAG刺激对压力感受性心动过缓的抑制作用。随后用于恢复5-羟色胺合成的5-羟色氨酸给药(60 mg / kg ip)使dPAG刺激对对氯苯丙氨酸预处理的大鼠的主动脉和苯肾上腺素引起的心脏反射反应的抑制作用得以恢复。另一方面,在未经预处理的大鼠中,预先通过NTS显微注射granisetron,5-HT(3)受体拮抗剂或双小分子GABA(A)可以显着降低dPAG刺激对心脏压力反射的抑制作用。 )受体拮抗剂。这些结果表明,5-羟色胺在dPAG刺激诱导的对心肌血管压力感受器反射反应的抑制中起关键作用。此外,他们支持NTS中的5-HT(3)和GABA(A)受体在下游抑制dPAG刺激引起的压力反射反应的想法。

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