Krstić M K
Department of Pharmacology, Faculty of Medicine, Belgrade, Yugoslavia.
Neuropharmacology. 1988 Dec;27(12):1215-9. doi: 10.1016/0028-3908(88)90022-6.
In pithed guinea-pigs, the general characteristics and origin of the pressor response to intravenous injection of histamine were examined. Histamine (5-80 micrograms/kg) produced a rapid, short-lasting, constant, prominent and dose-dependent pressor response, followed by a secondary slight and prolonged depressor response. The vascular response to histamine was accompanied by a marked tachycardia. The pressor effect of histamine (30 micrograms/kg) was strongly reduced or abolished in animals pretreated with nicotine, reserpine, bretylium or 6-hydroxydopamine. Furthermore, pyrilamine, a histamine H1-receptor antagonist, antagonized in a dose-dependent manner the pressor response to histamine. On the contrary, metiamide, a histamine H2-receptor antagonist, as well as hexamethonium and atropine, cholinergic antagonists, did not suppress the pressor effect of histamine. The present experiments provide evidence that in guinea-pigs, the pressor component of the vascular response to histamine results predominantly from the activation of histamine H1-receptors in the sympathetic ganglia with consequent release of noradrenaline at postganglionic sympathetic nerve terminals.
在脊髓被横断的豚鼠中，研究了静脉注射组胺后升压反应的一般特征和起源。组胺（5 - 80微克/千克）产生快速、短暂、持续、显著且剂量依赖性的升压反应，随后是继发性的轻微且持久的降压反应。组胺引起的血管反应伴有明显的心动过速。在用尼古丁、利血平、溴苄铵或6 - 羟基多巴胺预处理的动物中，组胺（30微克/千克）的升压作用显著降低或消除。此外，组胺H1受体拮抗剂吡苄明以剂量依赖性方式拮抗对组胺的升压反应。相反，组胺H2受体拮抗剂甲硫咪胺以及胆碱能拮抗剂六甲铵和阿托品并未抑制组胺的升压作用。本实验提供了证据表明，在豚鼠中，血管对组胺反应的升压成分主要源于交感神经节中组胺H1受体的激活，从而导致节后交感神经末梢释放去甲肾上腺素。
