Seki Y, Suzuki Y, Baskaya M K, Saito K, Takayasu M, Shibuya M, Sugita K
Department of Neurosurgery, Nagoya University School of Medicine, Japan.
Am J Physiol. 1995 Jul;269(1 Pt 2):H135-9. doi: 10.1152/ajpheart.1995.269.1.H135.
The cardiovascular responses to intracisternally administered pituitary adenylate cyclase-activating polypeptide (PACAP) were investigated and compared with those of vasoactive intestinal peptide (VIP) in anesthetized dogs. Intracisternal administration of 10 nmol of PACAP-27 increased mean arterial blood pressure (MABP) significantly with a simultaneous increase of plasma arginine vasopressin and epinephrine concentrations. Intracisternal administration of VIP increased plasma arginine vasopressin concentration significantly but caused no appreciable change in MABP. Systemic infusion of the nonpeptide vasopressin V1 receptor antagonist OPC-21268 did not inhibit the PACAP-27-induced increase in MABP, whereas phentolamine, an alpha-adrenoceptor blocker, reversed the increase. Intracisternal pretreatment with the vasopressin V1 receptor antagonist [Pmp1, Tyr(Me)2]Arg8-vasopressin also inhibited the increase. These findings suggest that PACAP has a central pressor action by increasing sympathetic outflow, which is probably mediated by the vasopressinergic neural network. PACAP seems to play important roles in hormonal and neural control of systemic circulation.
研究了在麻醉犬中,脑池内注射垂体腺苷酸环化酶激活多肽(PACAP)后的心血管反应,并与血管活性肠肽(VIP)的反应进行了比较。脑池内注射10 nmol的PACAP-27可显著升高平均动脉血压(MABP),同时血浆精氨酸加压素和肾上腺素浓度升高。脑池内注射VIP可显著升高血浆精氨酸加压素浓度,但对MABP无明显影响。全身输注非肽类加压素V1受体拮抗剂OPC-21268不能抑制PACAP-27诱导的MABP升高,而α-肾上腺素能受体阻滞剂酚妥拉明可逆转这种升高。用加压素V1受体拮抗剂[Pmp1,Tyr(Me)2]Arg8-加压素进行脑池内预处理也可抑制这种升高。这些发现表明,PACAP通过增加交感神经输出而具有中枢升压作用,这可能是由加压素能神经网络介导的。PACAP似乎在全身循环的激素和神经控制中起重要作用。