Murase T, Kondo K, Otake K, Oiso Y
First Department of Internal Medicine, Nagoya University School of Medicine, Japan.
Neuroendocrinology. 1993 Jun;57(6):1092-6. doi: 10.1159/000126475.
The effect of pituitary adenylate cyclase-activating polypeptide (PACAP) on arginine vasopressin (AVP) release was investigated in conscious rats. Intracerebroventricular (i.c.v.) administration of PACAP raised the plasma AVP concentration in a dose-dependent manner (50-500 pmol/rat), and the maximum effect was obtained at 5 min after the administration. This AVP-releasing effect was not due to a fall of blood pressure, increase of plasma Na or decrease of plasma volume, all of which are known to stimulate AVP release. PACAP had little effect on blood pressure at a low dose, but at higher doses increased it. Vasoactive intestinal peptide (VIP), which is homologous to PACAP, also raised the plasma AVP concentration by i.c.v. injection. An antagonist for VIP receptor, [Lys, Pro, Arg, Tyr]-VIP inhibited the VIP-induced increase of plasma AVP, but had little effect on PACAP-induced increase of plasma AVP. These results suggest that PACAP stimulates AVP release, via specific receptors which are distinct from VIP receptors.
在清醒大鼠中研究了垂体腺苷酸环化酶激活多肽（PACAP）对精氨酸加压素（AVP）释放的影响。脑室内（i.c.v.）注射PACAP可使血浆AVP浓度呈剂量依赖性升高（50 - 500 pmol/大鼠），给药后5分钟达到最大效应。这种AVP释放效应并非由于血压下降、血浆钠升高或血浆容量减少，而这些因素均已知可刺激AVP释放。低剂量的PACAP对血压影响不大，但高剂量时会使其升高。与PACAP同源的血管活性肠肽（VIP）通过脑室内注射也可提高血浆AVP浓度。VIP受体拮抗剂[Lys, Pro, Arg, Tyr]-VIP可抑制VIP诱导的血浆AVP升高，但对PACAP诱导的血浆AVP升高影响不大。这些结果表明，PACAP通过与VIP受体不同的特异性受体刺激AVP释放。
