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R. Muallem BSc R. Reimer PhD Dr. H. S. Odes MD M. Schwenk MD W. Beil MD K. -F. Sewing MD 《Digestive diseases and sciences》1994,39(5):1078-1084
The role of carbonic anhydrase in the process of proximal duodenal mucosal bicarbonate secretion was investigated in the guinea pig. In a series of experimentsin vivo, the duodenum was perfused with 24 mmol/liter NaHCO3 solution (+ NaCl for isotonicity) to ensure that active duodenal HCO
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secretion against a concentration gradient was measured. Acetazolamide (80 mg/kg) was infused intravenously to examine the role of carbonic anhydrase on basal and agonist-stimulated HCO
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secretion. Acetazolamide abolished basal HCO
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secretion and significantly decreased HCO
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secretion after stimulation with dibutyryl 5-cyclic adenosine monophosphate (dBcAMP, 10–5 mol/kg), dibutyryl 5-cyclic guanosine monophosphate (dBcGMP, 10–5 mol/kg), prostaglandin E2 (PGE2, 10–6 mol/kg), PGF2 (10–6 mol/kg), tetradecanoyl-phorbol-acetate (TPA, 10–7 mol/kg), glucagon (10–7 mol/kg), vasoactive intestinal polypeptide (VIP, 10–8 mol/kg), and carbachol (10–8 mol/kg). Utilizing a fluorescence technique, we could detect the enzyme carbonic anhydrase in equal amounts in villous and crypt cells of the proximal duodenal epithelium; no activity was demonstrated in tissues pretreated with acetazolamide. In conclusion, carbonic anhydrase is required for both basal and stimulated duodenal HCO
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secretion.This research was supported by the German-Israel Foundation for Scientific Research and Development, Grant Number I-78-054.2/88. 相似文献