血管加压素的抗伤害感受和体温调节作用对V1受体拮抗剂敏感。

Antinociceptive and thermoregulatory actions of vasopressin are sensitive to a V1-receptor antagonist.

作者信息

Oluyomi A O, Hart S L

机构信息

Biomedical Sciences Division, King's College, London, UK.

出版信息

Neuropeptides. 1992 Nov;23(3):137-42. doi: 10.1016/0143-4179(92)90113-b.

DOI:10.1016/0143-4179(92)90113-b

PMID:1470306

Abstract

The involvement of arginine vasopressin (AVP) has been investigated in cold water swim (CWS) stress-induced antinociception (SIA) and CWS-induced hypothermia. The antinociceptive action of AVP (0.5 micrograms, i.c.v.) pre-CWS was antagonized by d(CH2)5Tyr(Me)AVP (0.5 micrograms, i.c.v.) but not by naloxone (5 micrograms, i.c.v.). CWS produced SIA on the hot-plate which was initially naloxone-insensitive. Neither AVP nor its antagonist had any significant effect on CWS SIA. AVP-induced increase in body temperature, during recovery from CWS-induced hypothermia, was significantly (P < 0.001) reduced in the presence of its antagonist. These findings suggest that the antinociceptive and thermoregulatory actions of AVP may be mediated via V1-receptors.

摘要

精氨酸加压素（AVP）在冷水游泳（CWS）应激诱导的抗伤害感受（SIA）和CWS诱导的体温过低中的作用已得到研究。在CWS前给予AVP（0.5微克，脑室内注射）的抗伤害感受作用被d（CH2）5Tyr（Me）AVP（0.5微克，脑室内注射）拮抗，但不被纳洛酮（5微克，脑室内注射）拮抗。CWS在热板上产生SIA，最初对纳洛酮不敏感。AVP及其拮抗剂对CWS SIA均无显著影响。在从CWS诱导的体温过低恢复过程中，AVP诱导的体温升高在其拮抗剂存在下显著（P < 0.001）降低。这些发现表明，AVP的抗伤害感受和体温调节作用可能通过V1受体介导。