Takano Y, Nagashima A, Hagio T, Tateishi K, Kamiya H
Department of Pharmacology, Faculty of Pharmaceutical Sciences, School of Medicine, Fukuoka University, Japan.
Brain Res. 1990 Oct 1;528(2):231-7. doi: 10.1016/0006-8993(90)91662-z.
The mechanisms of action of tachykinin peptides thought to be involved in central cardiovascular regulation were examined. Intracerebroventricular injections (i.c.v.) of tachykinin peptides caused dose-dependent increases in blood pressure and heart rate. The pressor responses to substance P (SP) (10 micrograms, i.c.v.) and neurokinin A (NKA) (10 micrograms, i.c.v.) were blocked by peripheral administration of pentolinium or phentolamine, and partially attenuated by adrenalectomy. In contrast, the only initial pressor response to the neurokinin B (NKB) analogue senktide (10 micrograms, i.c.v.) was blocked by pentolinium or phentolamine. The pressor response to senktide was inhibited by pretreatment with a vasopressin V1 receptor antagonist (d(CH2)5OMe(Tyr)AVP) (10 micrograms/kg, i.v.), and senktide (10 micrograms, i.c.v.) caused an increase in plasma vasopressin level. However, the vasopressin antagonist did not influence the SP- and NKA-induced pressor responses. These results suggest that central SP and NKA increase the blood pressure and heart rate via sympathetic nerve activity, whereas central NKB increases the blood pressure mainly via release of vasopressin from the hypothalamus.
研究了被认为参与中枢心血管调节的速激肽类的作用机制。脑室内注射速激肽类可引起血压和心率的剂量依赖性升高。对P物质（SP）（10微克，脑室内注射）和神经激肽A（NKA）（10微克，脑室内注射）的升压反应可被潘托铵或酚妥拉明外周给药阻断，并因肾上腺切除术而部分减弱。相比之下，对神经激肽B（NKB）类似物速激肽（10微克，脑室内注射）的唯一初始升压反应可被潘托铵或酚妥拉明阻断。速激肽的升压反应可被血管加压素V1受体拮抗剂（d(CH2)5OMe(Tyr)AVP）（10微克/千克，静脉注射）预处理抑制，且速激肽（10微克，脑室内注射）可使血浆血管加压素水平升高。然而，血管加压素拮抗剂并不影响SP和NKA诱导的升压反应。这些结果表明，中枢SP和NKA通过交感神经活动升高血压和心率，而中枢NKB主要通过下丘脑释放血管加压素升高血压。
