Kimura T, Satoh S
Clin Exp Pharmacol Physiol. 1983 Sep-Oct;10(5):535-42. doi: 10.1111/j.1440-1681.1983.tb00222.x.
The effect of serotonin on cardiac sympathetic transmission was investigated in vagotomized and cardiac decentralized dogs. Administration of serotonin in doses of 10-100 micrograms/kg i.v., during the resting unstimulated state caused tachycardia and pressor responses which were inhibited by cyproheptadine but not by guanethidine. The tachycardia was reduced by a beta-adrenoceptor antagonist, bufetolol. Serotonin in doses of 3-100 micrograms/kg depressed the elevated heart rate during maintained electrical stimulation of the cardiac sympathetic nerves. Cyproheptadine did not antagonize the serotonin-induced depression of the stimulation-elevated heart rate, while desipramine attenuated but did not abolish it. Serotonin did not have a significant effect on the heart rate elevated by maintained infusion of noradrenaline. The present results suggest that serotonin-induced depression of heart rate during sympathetic nerve stimulation is due to presynaptic inhibition by serotonin of cardiac sympathetic transmission which is not mediated via 'classic' tryptaminergic receptors.
在切断迷走神经和使心脏去传入神经的犬中研究了5-羟色胺对心脏交感神经传递的作用。在静息未受刺激状态下,静脉注射剂量为10-100微克/千克的5-羟色胺会引起心动过速和升压反应,这些反应可被赛庚啶抑制,但不能被胍乙啶抑制。心动过速可被β-肾上腺素能受体拮抗剂布非洛尔减轻。剂量为3-100微克/千克的5-羟色胺可降低在持续电刺激心脏交感神经期间升高的心率。赛庚啶不能拮抗5-羟色胺引起的对刺激所致心率升高的抑制作用,而地昔帕明可减弱但不能消除这种作用。5-羟色胺对持续输注去甲肾上腺素引起的心率升高没有显著影响。目前的结果表明,交感神经刺激期间5-羟色胺引起的心率抑制是由于5-羟色胺对心脏交感神经传递的突触前抑制,这种抑制不是通过“经典”的色胺能受体介导的。