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首页> 外文期刊>American Journal of Physiology >Mutual dependence of VIP/PACAP and CCK receptor signaling for a physiological role in duck exocrine pancreatic secretion.
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Mutual dependence of VIP/PACAP and CCK receptor signaling for a physiological role in duck exocrine pancreatic secretion.

机译：VIP / PACAP和CCK受体信号转导在鸭外分泌胰腺分泌中的生理作用相互依赖。

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摘要

Unlike in rodents, CCK has not been established as a physiological regulator in avian exocrine pancreatic secretion. In the isolated duck pancreatic acini, 1 nM CCK was required for stimulation of amylase secretion, maximal effect being achieved at 10 nM; picomolar CCK was without effect. Vasoactive intestinal peptide (VIP)/pituitary adenylate cyclase activating peptide (PACAP) receptor (VPAC) agonists PACAP-38 and PACAP-27 (10(-12)-10(-7) M) alone had no effect, but made picomolar CCK effective. VPAC agonist VIP 10(-10)-10(-7) M stimulated amylase secretion marginally, but made CCK 10(-12)-10(-10) M effective also. PACAP-27 and VIP both shifted the maximal CCK concentration from 10(-8) to 10(-9) M. This sensitizing effect was mimicked by forskolin. CCK dose dependently induced intracellular Ca2+ concentration ([Ca2+]i) oscillations. PACAP-38 (1 nM), PACAP-27 (1 nM), VIP (10 nM), or forskolin (10 microM) alone did not stimulate [Ca2+]i increase, neither did they modulate CCK (1 nM)-induced oscillations; but when they were added to cells simultaneously exposed to subthreshold CCK (10 pM), calcium spikes emerged. Amylase secretion induced by the simultaneous presence of 10 pM CCK and VPAC agonists was completely blocked by removing extracellular calcium, but the protein kinase C inhibitor staurosporine (1 microM) was without effect. CCK (10 nM)-induced secretion was inhibited by CCK1 receptor antagonist FK480 (1 microM). Gastrin from 10(-12) to 10(-6) M did not stimulate amylase secretion nor did it (100 nM) induce [Ca2+]i increase. The above data suggest that duck pancreatic acini possess both CCK1 and VPAC receptors; simultaneous activation of both is required for each to play a physiological role.
机译：与啮齿动物不同，CCK尚未被确定为禽外分泌胰腺分泌的生理调节剂。在分离的鸭胰腺腺泡蛋白中，刺激淀粉酶分泌需要1 nM CCK，在10 nM时达到最大作用。皮摩尔CCK无效。血管活性肠肽（VIP）/垂体腺苷酸环化酶激活肽（PACAP）受体（VPAC）激动剂PACAP-38和PACAP-27（10（-12）-10（-7）M）单独无效，但使皮摩尔CCK有效。 VPAC激动剂VIP 10（-10）-10（-7）M略微刺激了淀粉酶的分泌，但也使CCK 10（-12）-10（-10）M有效。 PACAP-27和VIP都将最大CCK浓度从10（-8）移至10（-9）M。这种增敏作用被毛喉素所模仿。 CCK剂量依赖性地诱导细胞内Ca2 +浓度（[Ca2 +] i）振荡。仅PACAP-38（1 nM），PACAP-27（1 nM），VIP（10 nM）或毛喉素（10 microM）不会刺激[Ca2 +] i的增加，它们也不能调节CCK（1 nM）引起的振荡;但是，当将它们添加到同时暴露于亚阈值CCK（10 pM）的细胞中时，就会出现钙尖峰。通过同时存在10 pM CCK和VPAC激动剂诱导的淀粉酶分泌通过去除细胞外钙而被完全阻断，但是蛋白激酶C抑制剂星形孢菌素（1 microM）没有作用。 CCK1受体拮抗剂FK480（1 microM）抑制CCK（10 nM）诱导的分泌。胃泌素从10（-12）到10（-6）M不会刺激淀粉酶分泌，也不会（100 nM）诱导[Ca2 +] i增加。上述数据表明，鸭胰腺腺泡既具有CCK1受体又具有VPAC受体。两者都需要同时激活才能发挥生理作用。

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