Dehaye J P, Winand J, Damien C, Poloczek P, Svoboda M, Christophe J
Peptides. 1984 Mar-Apr;5(2):333-7. doi: 10.1016/0196-9781(84)90230-4.
The effects of Gila monster venom on dispersed rat pancreatic acini were compared with those of secretin and VIP. The efficacy of the venom in terms of amylase release was much higher (a 24-fold increase over basal secretion) than that of secretin (a 4-fold increase) and VIP (+ 40% only). On the other hand, cyclic AMP levels increased 12-fold with the venom, as compared to 18-fold with secretin and 16-fold with VIP. The venom, VIP and secretin all displaced 125I-VIP and the competition curve with the venom was steeper, suggesting that all VIP-recognizing receptors bound the venom with the same affinity. VIP receptors were, however, not responsible for the release of amylase provoked by the venom since VIP (and secretin) did not inhibit the secretory action of the venom. The venom exerted no effect on 45Ca efflux and its secretory effect did not depend on the presence of external calcium. Besides, the effect of CCK-8 on amylase release was additive with the effect of the venom. A first exposure to the venom induced a refractoriness to itself with respect to amylase release but not in terms of cyclic AMP increase. In conclusion, Gila monster venom may contain one component binding to VIP/secretin receptors with resulting cyclic AMP elevation. A second venom component may be responsible for the high secretory efficacy, without involving cyclic AMP or calcium efflux.
将吉拉毒蜥毒液对分散的大鼠胰腺腺泡的作用与促胰液素和血管活性肠肽（VIP）的作用进行了比较。就淀粉酶释放而言，毒液的效力（比基础分泌增加24倍）远高于促胰液素（增加4倍）和VIP（仅增加40%）。另一方面，毒液使环磷酸腺苷（cAMP）水平增加了12倍，相比之下，促胰液素使其增加18倍，VIP使其增加16倍。毒液、VIP和促胰液素均能置换125I-VIP，且毒液的竞争曲线更陡，这表明所有识别VIP的受体与毒液的结合亲和力相同。然而，VIP受体并非毒液引发淀粉酶释放的原因，因为VIP（和促胰液素）并未抑制毒液的分泌作用。毒液对45Ca外流没有影响，其分泌作用也不依赖于细胞外钙的存在。此外，胆囊收缩素-8（CCK-8）对淀粉酶释放的作用与毒液的作用具有相加性。首次接触毒液会使其自身对淀粉酶释放产生耐受性，但对cAMP增加方面无此影响。总之，吉拉毒蜥毒液可能含有一种与VIP/促胰液素受体结合的成分，导致cAMP升高。第二种毒液成分可能是其高分泌效力的原因，且不涉及cAMP或钙外流。
