Arruebo M P, Sorribas V, Rodriguez-Yoldi M J, Murillo M D, Alcalde A I
Departamento de Biomedicina, Fisiología, Facultad de Veterinaria, Universidad de Zaragoza, Spain.
Zentralbl Veterinarmed A. 1990 Mar;37(2):123-9. doi: 10.1111/j.1439-0442.1990.tb00883.x.
The vasoactive intestinal peptide (VIP) has shown to be widely distributed in the gastrointestinal mucosa, submucosa and nerves, and the existence of VIP receptors on the basolateral membrane of enterocytes has been recently reported for many species. The interaction of VIP with its receptors seemed to increase cyclic AMP level, and this nucleotide has been shown to be responsible for the intestinal secretion produced by VIP. The present study confirms that VIP inhibits the intestinal absorption of D-galactose. This effect seems to be due to the inhibition of the Na(+)-independent basolateral intestinal sugar transport system. RMI 12330A, described as adenylate cyclase inhibitors, blocked the VIP action. These findings suggest that cyclic AMP might be responsible for the inhibition of Na(+)-independent transport of D-galactose across the basolateral membrane. Moreover, results obtained to determine the possible role of calcium in the action of VIP suggest that Ca2+ play a part, directly or indirectly, in the inhibition of the D-galactose transport across the basolateral membrane produced by VIP.
血管活性肠肽(VIP)已被证明广泛分布于胃肠道黏膜、黏膜下层和神经中,最近有报道称许多物种的肠上皮细胞基底外侧膜上存在VIP受体。VIP与其受体的相互作用似乎会增加环磷酸腺苷(cAMP)水平,并且这种核苷酸已被证明是VIP产生肠道分泌的原因。本研究证实,VIP会抑制D-半乳糖的肠道吸收。这种作用似乎是由于抑制了不依赖于Na⁺的基底外侧肠道糖转运系统。RMI 12330A,一种被描述为腺苷酸环化酶抑制剂的物质,阻断了VIP的作用。这些发现表明,环磷酸腺苷可能是抑制D-半乳糖跨基底外侧膜进行不依赖于Na⁺转运的原因。此外,为确定钙在VIP作用中可能发挥的作用而获得的结果表明,Ca²⁺直接或间接参与了VIP对D-半乳糖跨基底外侧膜转运的抑制作用。