Quebbemann B B, Rivier J, Bache R J
Department of Medicine, University of Minnesota, Minneapolis 55455.
Peptides. 1991 Sep-Oct;12(5):989-93. doi: 10.1016/0196-9781(91)90048-t.
Intracoronary infusion of [4Cl-D-Phe6-Leu17]VIP caused modest significant inhibition of the coronary vasodilation produced by intraarterial VIP, but did not significantly inhibit serotonin-induced coronary vasodilation. In addition, infusion of [4Cl-D-Phe6-Leu17]VIP did not result in significant changes in baseline coronary resistance, heart rate or left ventricular dP/dt. These findings demonstrate that [4Cl-D-Phe6-Leu17]VIP is a competitive antagonist of VIP-induced vasodilation in the canine coronary circulation, but fail to demonstrate a significant role for VIP in the regulation of resting coronary vasomotor tone, and do not support the hypothesis that VIP is a mediator of serotonin-induced coronary arteriolar dilation.
冠状动脉内注入[4-氯-D-苯丙氨酸6-亮氨酸17]血管活性肠肽（VIP）对动脉内注入VIP所引起的冠状动脉舒张有适度但显著的抑制作用，但对血清素诱导的冠状动脉舒张无显著抑制作用。此外，注入[4-氯-D-苯丙氨酸6-亮氨酸17]VIP并未导致冠状动脉基线阻力、心率或左心室dp/dt发生显著变化。这些发现表明，[4-氯-D-苯丙氨酸6-亮氨酸17]VIP是犬冠状动脉循环中VIP诱导的血管舒张的竞争性拮抗剂，但未能证明VIP在静息冠状动脉血管舒缩张力调节中起重要作用，也不支持VIP是血清素诱导的冠状动脉小动脉舒张介质的假说。
