Nakayama Y, Takano Y, Saito R, Kamiya H
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Japan.
Brain Res. 1992 Nov 13;595(2):339-42. doi: 10.1016/0006-8993(92)91069-q.
The central pressor actions of the tachykinin NK-3 receptor in the paraventricular nucleus (PVN) of the hypothalamus were examined in anesthetized rats. In forebrain-restricted animals, the selective tachykinin NK-3 receptor agonist senktide (10 micrograms, i.c.v.) increased the blood pressure, and this pressor response was more potent than in control animals. Injection of senktide into the PVN also increased the blood pressure, and this pressor response was inhibited by pretreatment with the vasopressin V1 receptor antagonist (10 micrograms/kg, i.v.). These results suggest that central injection of senktide stimulated the NK-3 receptor in the PVN of the hypothalamus, and increased blood pressure by inducing release of vasopressin from the pituitary gland.
在麻醉大鼠中研究了下丘脑室旁核（PVN）中速激肽NK-3受体的中枢升压作用。在前脑受限的动物中，选择性速激肽NK-3受体激动剂senktide（10微克，脑室内注射）可升高血压，且这种升压反应比对照动物更强。将senktide注射到PVN中也可升高血压，而这种升压反应可被血管加压素V1受体拮抗剂（10微克/千克，静脉注射）预处理所抑制。这些结果表明，脑室内注射senktide可刺激下丘脑PVN中的NK-3受体，并通过诱导垂体释放血管加压素而升高血压。
