Petersen K U, Wood J R, Schulze G, Heintze K
J Membr Biol. 1981;62(3):183-93. doi: 10.1007/BF01998164.
Gallbladder fluid and electrolyte transport was investigated in vitro. In guinea pig gallbladder, equimolar substitution of acetate, propionate, butyrate or valerate for HCO3 was increasingly effective in stimulating fluid absorption. The stimulatory potency of these compounds was a function of their chloroform water partition coefficients. The stimulatory effects of the isomers isobutyrate and isovalerate were less than predicted from their partition coefficients. Acidification of the gallbladder lumen, however, was strictly dependent on the partition coefficients for all of the above fatty acids. Unidirectional 22Na fluxes were measured in rabbit and guinea pig gallbladders under short-circuit conditions. In the presence of butyrate stimulation of net Na flux was due entirely to an increase in the mucosal-to-serosal Na flux. Stimulation by butyrate was abolished by its omission from the mucosal bathing solution. The transepithelial electrical potential difference in both rabbit and guinea pig gallbladder became more lumen positive following mucosal but not serosal addition of butyrate. Net 14C-butyrate fluxes were too small to account for stimulation of Na absorption in either species. Butyrate stimulation of Na absorption by guinea pig gallbladder was abolished by increasing the bathing pH from 7.4 to 8.1. Tris buffer (25 mM) partially inhibited butyrate-dependent gallbladder fluid absorption by rabbit and guinea pig at pH 6.4 and 7.0, respectively, and completely at pH 8.4. These results reveal a marked similarity between butyrate and HCO stimulation of gallbladder NaCl and fluid absorption. The results are best explained by a double ion-exchange model, in which butyrate (HCO3) in the mucosal solution acts to maintain the intracellular supply of H+ and butyrate (HCO3) for countertransport of Na and Cl, respectively.
对胆囊的液体和电解质转运进行了体外研究。在豚鼠胆囊中，用乙酸盐、丙酸盐、丁酸盐或戊酸盐等摩尔替代HCO₃对刺激液体吸收的效果越来越显著。这些化合物的刺激效力与其氯仿 - 水分配系数有关。异丁酸盐和异戊酸盐异构体的刺激作用低于根据其分配系数所预测的效果。然而，胆囊腔内的酸化严格取决于上述所有脂肪酸的分配系数。在短路条件下测量了兔和豚鼠胆囊中的单向²²Na通量。在丁酸盐存在的情况下，净Na通量的刺激完全归因于黏膜到浆膜的Na通量增加。从黏膜浴液中去除丁酸盐后，其刺激作用消失。在兔和豚鼠胆囊中，黏膜而非浆膜添加丁酸盐后，跨上皮电位差变得更加向腔内为正。净¹⁴C - 丁酸盐通量太小，无法解释两种动物中Na吸收的刺激情况。将浴液pH从7.4提高到8.1可消除丁酸盐对豚鼠胆囊Na吸收的刺激作用。Tris缓冲液（25 mM）分别在pH 6.4和7.0时部分抑制兔和豚鼠胆囊中丁酸盐依赖的液体吸收，在pH 8.4时完全抑制。这些结果揭示了丁酸盐和HCO对胆囊NaCl和液体吸收刺激之间的显著相似性。这些结果最好用双离子交换模型来解释，其中黏膜溶液中的丁酸盐（HCO₃）分别作用于维持细胞内H⁺和丁酸盐（HCO₃）的供应，用于Na和Cl的反向转运。
