Odes H S, Muallem R, Reimer R, Beil W, Schwenk M, Sewing K F
Gastroenterology Institute, Soroka Medical Center, Beer Sheva, Israel.
Am J Physiol. 1993 Aug;265(2 Pt 1):G270-6. doi: 10.1152/ajpgi.1993.265.2.G270.
Although it is well known that vagal stimulation induces duodenal HCO3- secretion, there is presently no information about the nature of the cholinoceptor and the intracellular signals involved. In a series of experiments performed in a guinea pig duodenal loop model in situ, intravenous carbachol, atropine, pirenzepine, and hexamethonium were used to determine the extent of cholinergic stimulation and the types of cholinoceptors. Carbachol (2 micrograms.kg-1.5 min-1) stimulated HCO3- secretion threefold, and atropine (0.1 mg.kg-1.5 min-1) and pirenzepine (1 mg.kg-1.5 min-1) both abolished this effect. In addition, hexamethonium (0.3 mg.kg-1.5 min-1) inhibited carbachol-stimulated duodenal HCO3- secretion. Vasoactive intestinal peptide (VIP, 5 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, and this action was partly inhibited by atropine (0.1 mg.kg-1.5 min-1) but not by pirenzepine (1 mg.kg-1.5 min-1). [4Cl-D-Phe6,Leu17]VIP (3.3 mg/kg), an antagonist to VIP, reduced basal, VIP-stimulated, and carbachol-stimulated HCO3- secretion. To examine the role of Ca2+ in this process, Ca2+ ionophore A23187, verapamil, and nifedipine were employed. A23187 (5, 50, 500 micrograms.kg-1.5 min-1) stimulated duodenal HCO3- secretion, an effect blocked by the VIP antagonist, and modestly augmented the effect of carbachol. Verapamil (0.2 mg.kg-1.5 min-1) and nifedipine (1.7 mg.kg-1.5 min-1) stopped the effect of carbachol on duodenal HCO3- secretion. These results suggest, that in cholinergic regulation of duodenal HCO3- secretion, the M-cholinoceptor pathway, Ca2+, and VIP are involved.
虽然众所周知迷走神经刺激可诱导十二指肠HCO₃⁻分泌，但目前尚无关于所涉及的胆碱能受体性质和细胞内信号的信息。在一系列在豚鼠十二指肠肠袢原位模型中进行的实验中，静脉注射卡巴胆碱、阿托品、哌仑西平和六甲铵，以确定胆碱能刺激的程度和胆碱能受体的类型。卡巴胆碱（2微克·千克⁻¹·5分钟⁻¹）使HCO₃⁻分泌增加了两倍，阿托品（0.1毫克·千克⁻¹·5分钟⁻¹）和哌仑西平（1毫克·千克⁻¹·5分钟⁻¹）均消除了这种作用。此外，六甲铵（0.3毫克·千克⁻¹·5分钟⁻¹）抑制了卡巴胆碱刺激的十二指肠HCO₃⁻分泌。血管活性肠肽（VIP，5微克·千克⁻¹·5分钟⁻¹）刺激十二指肠HCO₃⁻分泌，这种作用部分被阿托品（0.1毫克·千克⁻¹·5分钟⁻¹）抑制，但不被哌仑西平（1毫克·千克⁻¹·5分钟⁻¹）抑制。[4Cl-D-Phe6,Leu17]VIP（3.3毫克/千克），一种VIP拮抗剂，降低了基础、VIP刺激和卡巴胆碱刺激的HCO₃⁻分泌。为了研究Ca²⁺在此过程中的作用，使用了Ca²⁺离子载体A23187、维拉帕米和硝苯地平。A23187（5、50、500微克·千克⁻¹·5分钟⁻¹）刺激十二指肠HCO₃⁻分泌，这种作用被VIP拮抗剂阻断，并适度增强了卡巴胆碱的作用。维拉帕米（0.2毫克·千克⁻¹·5分钟⁻¹）和硝苯地平（1.7毫克·千克⁻¹·5分钟⁻¹）阻断了卡巴胆碱对十二指肠HCO₃⁻分泌的作用。这些结果表明，在十二指肠HCO₃⁻分泌的胆碱能调节中，M胆碱能受体途径、Ca²⁺和VIP均参与其中。
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