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中枢H1和H2受体在高渗、低血容量及中枢胆碱能刺激诱导的饮水行为中的作用。

Involvement of central H1 and H2 receptors in water intake induced by hyperosmolarity, hypovolemia and central cholinergic stimulation.

作者信息

Magrani Janeide, de Castro E Silva Emilio, Athanazio Rodrigo, Improta Lilia, Fregoneze Josmara B

机构信息

Department of Physiology, Health Sciences Institute, Federal University of Bahia, 40110-100 Salvador-Bahia, Brazil.

出版信息

Physiol Behav. 2006 Sep 30;89(2):241-9. doi: 10.1016/j.physbeh.2006.06.004. Epub 2006 Jul 17.

Abstract

In the present study we investigated the participation of central H1 and H2 histaminergic receptors in water intake induced by hyperosmolarity (evoked by intragastric salt load), by hypovolemia (promoted by the subcutaneous administration of polyethyleneglycol) and by the pharmacological stimulation of central cholinergic pathways by the muscarinic agonist carbachol in male Wistar rats. The data presented here show that the pharmacological blockade of central H1 histaminergic receptors by third ventricle injections of mepyramine significantly decreased water intake induced by hyperosmolarity, hypovolemia and by the intracerebroventricular injections of carbachol. On the other hand, the pharmacological blockade of central H2 histaminergic receptors by third ventricle injections of cimetidine significantly reduced water intake in hypovolemic and hyperosmotic animals, but failed to alter water intake induced by central cholinergic stimulation by carbachol. We conclude that H1 and H2 brain histaminergic receptors are involved in inducing thirst during hyperosmolarity and hypovolemia and that H1 histaminergic receptors located post-synaptically in relation to cholinergic pathways seem to be important in triggering drinking following central pharmacological cholinergic stimulation.

摘要

在本研究中,我们调查了雄性Wistar大鼠中枢H1和H2组胺能受体在高渗(由胃内盐负荷诱发)、低血容量(由皮下注射聚乙二醇促进)以及毒蕈碱激动剂卡巴胆碱对中枢胆碱能途径的药理学刺激所诱导的饮水行为中的参与情况。此处呈现的数据表明,通过向第三脑室注射美吡拉敏对中枢H1组胺能受体进行药理学阻断,可显著降低高渗、低血容量以及脑室内注射卡巴胆碱所诱导的饮水量。另一方面,通过向第三脑室注射西咪替丁对中枢H2组胺能受体进行药理学阻断,可显著减少低血容量和高渗动物的饮水量,但未能改变卡巴胆碱对中枢胆碱能刺激所诱导的饮水量。我们得出结论,H1和H2脑组胺能受体参与了高渗和低血容量期间的口渴诱导,并且相对于胆碱能途径位于突触后的H1组胺能受体似乎在中枢药理学胆碱能刺激后引发饮水行为中起重要作用。

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