Bridén S, Flemström G
Department of Physiology and Medical Biophysics, Uppsala University Biomedical Centre, Sweden.
Acta Physiol Scand. 1989 Dec;137(4):481-7. doi: 10.1111/j.1748-1716.1989.tb08784.x.
Proximal duodenum from the amphibian Necturus was stripped of muscle layers and the mucosa was mounted as a tube for studies of alkali transport or as a flat sheet for intracellular impalement by voltage-sensitive glass micro-electrodes. The mucosa alkalinized the unbuffered luminal perfusate at a high rate (3.4 muequiv. cm-1 h-1) and developed a transepithelial electric potential difference of 5.7 mV (lumen negative). Transport was inhibited by 2,4-dinitrophenol (10(-4) M) and by furosemide (10(-3) M) and SITS (10(-3) M) on the seros but not on the mucosal side, indicating dependence on tissue metabolism and on serosal membrane Cl-/HCO3- exchange. Prostaglandin E2 (10(-7)-10(-5) M) and dibutyryl cyclic AMP (10(-6)-10(-4) M) had no effects on the secretion or transepithelial electrical potential difference. removal of serosal HCO3- decreased luminal alkalinization by 75%, indicating a contribution by passive migration of HCO3- and/or a dependence of transcellular transport on the nutrient supply of this ion. Administration of HCO3- (17.8 mM) to the luminal perfusate affected neither the transepithelial nor transmembrane electrical potential differences nor the resistance ratio. It is thus unlikely that the luminal membrane possesses any major HCO3- conductance.
将两栖动物泥螈的十二指肠近端去除肌肉层，将黏膜制成管状用于碱转运研究，或制成平板用于电压敏感玻璃微电极进行细胞内刺入研究。黏膜以高速率（3.4微当量·厘米⁻¹·小时⁻¹）使无缓冲的腔内灌流液碱化，并产生5.7毫伏的跨上皮电位差（腔面为负）。转运受到2,4-二硝基苯酚（10⁻⁴摩尔/升）、呋塞米（10⁻³摩尔/升）和SITS（10⁻³摩尔/升）的抑制，但仅在浆膜侧，黏膜侧不受影响，表明其依赖于组织代谢和浆膜Cl⁻/HCO₃⁻交换。前列腺素E₂（10⁻⁷ - 10⁻⁵摩尔/升）和二丁酰环磷酸腺苷（10⁻⁶ - 10⁻⁴摩尔/升）对分泌或跨上皮电位差无影响。去除浆膜侧的HCO₃⁻使腔内碱化降低75%，表明HCO₃⁻的被动迁移有作用和/或跨细胞转运依赖于该离子的营养供应。向腔内灌流液中加入HCO₃⁻（17.8毫摩尔/升）对跨上皮和跨膜电位差以及电阻比均无影响。因此，腔面膜不太可能具有任何主要的HCO₃⁻电导。
