Király A, Sütó G, Guth P, Taché Y
CURE/Digestive Disease Research Center, West Los Angeles VA Medical Center, California 90073, USA.
Peptides. 1997;18(9):1321-5. doi: 10.1016/s0196-9781(97)00208-8.
The specific VIP receptor antagonist, [4Cl-D-Phe6,Leu17]VIP, infused i.v. blocked close-intra-arterial infusion of VIP-induced increase in gastric mucosal blood flow (GMBF, measured by the hydrogen gas clearance), and decrease in mean arterial blood pressure while not influencing basal levels in urethane-anesthetized rats. The thyrotropin-releasing hormone (TRH) stable analog, RX 77368, injected intracisternally (IC, 30 ng) increased GMBF and blood pressure. The VIP antagonist did not significantly reduce the GMBF response to IC RX 77368 while enhancing the rise in blood pressure. These findings indicate that [4Cl-D-Phe6,Leu17]VIP is an antagonist for exogenous VIP-induced gastric hyperemia and hypotension and that VIP modulates the systemic blood pressure response to IC RX 77368 at 30 ng while not playing a primary role in the increase of GMBF.
特异性血管活性肠肽（VIP）受体拮抗剂[4Cl-D-Phe6,Leu17]VIP静脉注射，可阻断动脉内近距离注射VIP所诱导的胃黏膜血流量增加（通过氢气清除率测量胃黏膜血流量）以及平均动脉血压降低，而对氨基甲酸乙酯麻醉大鼠的基础水平无影响。促甲状腺激素释放激素（TRH）的稳定类似物RX 77368经脑池内注射（IC，30 ng）可增加胃黏膜血流量和血压。VIP拮抗剂不会显著降低对脑池内注射RX 77368的胃黏膜血流量反应，却会增强血压升高。这些发现表明，[4Cl-D-Phe6,Leu17]VIP是外源性VIP诱导的胃充血和低血压的拮抗剂，并且VIP在30 ng时调节对脑池内注射RX 77368的全身血压反应，但在胃黏膜血流量增加中不发挥主要作用。
