Vasoactive intestinal peptide (VIP) receptor (VPAC1, VPAC2) abundances in the myometrium and functions in the regulation of inflamed uterine contractility in pigs were studied. In the CON group with gilts, only laparotomy was performed. The gilts of SAL- and E. coli-treated groups were administered saline or E. coli into the uterine horns, respectively. The E. coli-induced endometritis resulted in a lesser myometrial relative abundance of VPAC1 and VPAC2 receptor mRNA transcripts and larger abundance of protein for these receptors. In the myometrium, treatment with VIP resulted in a lesser contractility amplitude than in the tissues of the CON- and SAL- and E. coli-treated groups and in frequency in the CON- and E.coli-treated group compared to the period before VIP treatment. Compared to when there was VIP treatment alone, treatment with VPAC1 and VPAC2 receptor antagonists resulted in a lesser inhibitory effect of VIP on contractility amplitude in the myometrium of the CON and SAL-treated groups and there was complete abolishment of the inhibitory VIP effect on frequency of myometrial contractility of the CON group. In the myometrium of E. coli-treated group, treatment with VPAC1 and VPAC2 receptor antagonists resulted in a reversal of the inhibitory effect of VIP on contractility amplitude, while treatment with VPAC2 receptor antagonist resulted in elimination of contractility and a lesser endometrium/myometrium inhibitory effect of VIP on frequency of these contractions. Results indicate VIP functions to decrease myometrial contractility of the inflamed pig uterus by having functions at VPAC1 and VPAC2 receptors.

研究了子宫肌层中血管活性肠肽 (VIP) 受体 (VPAC1、VPAC2) 的丰度以及在猪炎症性子宫收缩力的调节中的功能。在有小母猪的 CON 组中，只进行了剖腹手术。SAL-和大肠杆菌-治疗组的小母猪分别被施用盐水或大肠杆菌进入子宫角。该大肠杆菌诱导的子宫内膜炎导致 VPAC1 和 VPAC2 受体 mRNA 转录物的子宫肌层相对丰度较低，而这些受体的蛋白质丰度较高。在子宫肌层中，与 CON 和 SAL 以及大肠杆菌治疗组的组织相比，VIP 治疗导致的收缩幅度和 CON 和大肠杆菌治疗组的收缩率均低于之前的时期贵宾待遇。与单独使用 VIP 治疗相比，使用 VPAC1 和 VPAC2 受体拮抗剂治疗导致 VIP 对 CON 和 SAL 治疗组子宫肌层收缩幅度的抑制作用较小，并且完全消除了 VIP 对频率的抑制作用CON 组的子宫肌层收缩力。在大肠杆菌的子宫肌层中-治疗组，用 VPAC1 和 VPAC2 受体拮抗剂治疗导致 VIP 对收缩幅度的抑制作用逆转，而用 VPAC2 受体拮抗剂治疗导致收缩力消除和 VIP 对这些频率的较小子宫内膜/子宫肌层抑制作用宫缩。结果表明 VIP 功能通过在 VPAC1 和 VPAC2 受体上起作用来降低发炎猪子宫的子宫肌层收缩力。