Foster E S, Sandle G I, Hayslett J P, Binder H J
Gastroenterology. 1983 Feb;84(2):324-30.
To determine whether cyclic adenosine monophosphate influences active potassium transport in the rat colon, we studied the effect of dibutyryl cyclic adenosine monophosphate and theophylline on unidirectional transmural 42K fluxes across proximal colonic mucosa under short-circuited conditions. Active potassium secretion (-0.19 +/- 0.02 microEq/h X cm2) was present in animals maintained on a normal potassium diet. Both 0.5 mM dibutyryl cyclic adenosine monophosphate and 5 mM theophylline significantly increased net potassium secretion by 0.49 +/- 0.04 and 0.33 +/- 0.03 microEq/h X cm2, p less than 0.001, respectively; the stimulation of net potassium secretion was secondary to an increase in serosal-to-mucosal potassium transport without change in mucosal-to-serosal potassium movement. A similar increase in active potassium secretion (from -0.15 +/- 0.03 to -0.32 +/- 0.03 microEq/h X cm2, p less than 0.005) was produced by bethanechol, a cholinergic muscarinic agonist that alters sodium and chloride transport by a noncyclic adenosine monophosphate, calcium-dependent process. In animals maintained on a high potassium diet, active potassium secretion was significantly increased to -0.79 +/- 0.17 microEq/h X cm2 (p less than 0.001). In these potassium-loaded animals, theophylline produced a greater increase in active potassium secretion (0.91 +/- 0.10 vs. 0.33 +/- 0.03 microEq/h X cm2, p less than 0.001) than in animals fed a normal potassium diet. These studies demonstrate that cyclic adenosine monophosphate and noncyclic adenosine monophosphate mediated secretogogues stimulate active potassium secretion. We speculate that the mechanism by which cyclic adenosine monophosphate increases active potassium secretion is related to an increase in luminal potassium conductance.
为了确定环磷酸腺苷是否影响大鼠结肠中的活性钾转运,我们研究了二丁酰环磷酸腺苷和茶碱对短路条件下近端结肠黏膜单向跨壁(^{42}K)通量的影响。以正常钾饮食饲养的动物存在活性钾分泌((-0.19\pm0.02)微当量/小时×平方厘米)。(0.5)毫摩尔/升的二丁酰环磷酸腺苷和(5)毫摩尔/升的茶碱均显著增加净钾分泌,分别增加了(0.49\pm0.04)和(0.33\pm0.03)微当量/小时×平方厘米,(p\lt0.oooo1);净钾分泌的刺激是由于浆膜到黏膜的钾转运增加,而黏膜到浆膜的钾转运没有变化。毒蕈碱胆碱能激动剂贝胆碱通过非环磷酸腺苷、钙依赖过程改变钠和氯的转运,也产生了类似的活性钾分泌增加(从(-0.15\pm0.03)增加到(-0.32\pm0.03)微当量/小时×平方厘米,(p\lt0.005))。以高钾饮食饲养的动物,活性钾分泌显著增加至(-0.79\pm0.17)微当量/小时×平方厘米((p\lt0.001))。在这些钾负荷动物中,茶碱对活性钾分泌的增加幅度((0.91\pm0.10)与(0.33\pm0.03)微当量/小时×平方厘米相比,(p\lt0.001))大于以正常钾饮食饲养的动物。这些研究表明,环磷酸腺苷和非环磷酸腺苷介导的促分泌剂刺激活性钾分泌。我们推测环磷酸腺苷增加活性钾分泌的机制与管腔钾电导增加有关。