Modulation of bicarbonate secretion in rabbit duodenum: the role of calcium.
Modulation of bicarbonate secretion in rabbit duodenum: the role of calcium.
复制标题
兔十二指肠碳酸氢盐分泌的调节：钙的作用。
DOI：
10.1023/a:1018836407044
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发表时间：
1998
影响因子：
3.1
通讯作者：
Isenberg,JI
中科院分区：
文献类型：
--
作者：
Hogan,DL;Yao,B;Isenberg,JI
表面上皮性碳酸氢盐分泌物保护十二指肠近端免受酸性消化性损伤。环状一磷酸腺苷和钙作为肠道运输的细胞内介质。实验研究钙是否参与十二指肠碳酸氢盐的转运。在实验室中对兔十二指肠粘膜剥离进行了研究。钙离子载体A23187、卡巴胆碱、血管活性肠肽、前列腺素E_2、二丁酰环磷酸腺苷和电场刺激都能刺激HCO3转运。A23187刺激HCO3分泌和ISC；河豚毒素不能抑制这一作用。钙通道阻滞剂维拉帕米可阻断卡巴胆碱、血管活性肠肽和电场刺激引起的HCO3分泌，但不能改变前列腺素E_2或二丁酰环腺苷单磷酸刺激的基础HCO3分泌。因此，在卡巴胆碱、血管活性肠肽和电场刺激刺激十二指肠上皮HCO3转运的过程中，可能需要钙。前列腺素E_2和二丁酰环磷酸腺苷似乎通过钙非依赖性途径激活十二指肠HCO3的分泌(S)。
Surface epithelial bicarbonate secretionprotects the proximal duodenum from acid peptic injury.Cyclic adenosine monophosphate and calcium serve asintracellular mediators of intestinal transport.Experiments were performed to examine whether calciumparticipates in duodenal bicarbonate transport. Strippedduodenal mucosa from rabbits was studied in Ussingchambers. HCO3-transport wasstimulated by the calcium ionophore A23187, carbachol, vasoactiveintestinal peptide, prostaglandin E2,dibutyryl-cyclic adenosine monophosphate, and electricalfield stimulation. A23187 stimulatedHCO3-secretion andISC; tetrodotoxin failed to inhibit this effect. Thecalcium-channel blocker verapamil abolishedHCO3-secretion stimulated bycarbachol, vasoactive intestinal peptide, and electricalfield stimulation, but failed to alter basal, prostaglandin E2- ordibutyryl-cyclic adenosine monophosphate-stimulatedHCO3-secretion. Therefore,calcium is likely required during stimu lation ofduodenal epithelial HCO3-transport by carbachol, vasoactive intestinal peptide, and electricalfield stimulation. Prostaglandin E2- anddibutyryl-cyclic adenosine monophosphate appear toactivate duodenal HCO3-secretionby a calcium-independent pathway(s).