大鼠（褐家鼠）结肠中碳酸氢盐分泌的机制。

Mechanism of bicarbonate secretion in rat (Rattus rattus) colon.

Dagher P C, Rho J I, Charney A N

Nephrology Section, Department of Veterans Affairs Medical Center, New York University School of Medicine, NY 10010.

Comp Biochem Physiol Comp Physiol. 1993 May;105(1):43-8. doi: 10.1016/0300-9629(93)90171-y.

Abstract

Colonic HCO3 secretion was measured as the residual flux in male Sprague-Dawley rats (Rattus rattus). 2. Basal HCO3 secretion was increased by 1 mM dibutyryl cyclic AMP (dbcAMP) and was reduced to baseline by 0.1 mM methazolamide (Mtz) but not by SITS (1 mM), DIDS (1 mM) or amiloride (1 mM). 3. In vivo, intravenous vasoactive intestinal peptide increased HCO3 secretion and prior perfusion with 1 mM Mtz prevented this increase. 4. These results suggest that the source of basal and cAMP-stimulated HCO3 secretion is, in part, intracellular and requires the action of carbonic anhydrase.

摘要

在雄性斯普拉格-道利大鼠（褐家鼠）中，结肠碳酸氢根（HCO₃）分泌被测定为残余通量。2. 基础HCO₃分泌通过1 mM二丁酰环磷腺苷（dbcAMP）增加，并通过0.1 mM甲酰唑胺（Mtz）降至基线水平，但不受1 mM 4-乙酰氨基-4'-异硫氰酸基芪-2,2'-二磺酸（SITS）、1 mM 4,4'-二异硫氰酸基芪-2,2'-二磺酸（DIDS）或1 mM阿米洛利的影响。3. 在体内，静脉注射血管活性肠肽可增加HCO₃分泌，预先用1 mM Mtz灌注可阻止这种增加。4. 这些结果表明，基础和环磷腺苷（cAMP）刺激的HCO₃分泌部分来源于细胞内，并且需要碳酸酐酶的作用。