Hardcastle J, Hardcastle P T, Noble J M
J Physiol. 1983 Nov;344:69-80. doi: 10.1113/jphysiol.1983.sp014924.
The addition of BaCl2 to the serosal solution, at concentrations from 0 X 25 mM to 10 mM, caused increases in potential difference, short-circuit current and resistance across stripped sheets of rat mid-intestine, although mucosal application had little effect. The response to BaCl2 was significantly greater than that obtained with the same concentration of CaCl2. An increase in net Cl- secretion entirely accounted for the rise in short-circuit current induced by BaCl2. BaCl2 inhibited net fluid uptake by everted sacs. It also enhanced the accumulation of fluid by intestinal loops in vivo and this was associated with an increased potential difference. The response to BaCl2 in vitro was not reduced in the absence of serosal Ca2+ ions. The effect of BaCl2 was abolished by trifluoperazine and also by TMB-8 (8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride). BaCl2 did not alter cyclic AMP production by isolated enterocytes. It is concluded that BaCl2 induces intestinal secretion by releasing Ca2+ from intracellular stores which then combines with calmodulin to stimulate the secretory process.
向浆膜溶液中添加浓度为0.25 mM至10 mM的BaCl2,可使大鼠中肠剥离片的电位差、短路电流和电阻增加,尽管向黏膜施加时影响很小。BaCl2引起的反应明显大于相同浓度CaCl2所产生的反应。净Cl-分泌的增加完全解释了BaCl2诱导的短路电流的升高。BaCl2抑制外翻囊的净液体摄取。它还增强了体内肠袢的液体蓄积,这与电位差增加有关。在浆膜缺乏Ca2+离子的情况下,体外对BaCl2的反应并未减弱。三氟拉嗪和TMB-8(8-(N,N-二乙氨基)-辛基-3,4,5-三甲氧基苯甲酸盐酸盐)均可消除BaCl2的作用。BaCl2不会改变分离的肠上皮细胞的环磷酸腺苷生成。结论是,BaCl2通过从细胞内储存中释放Ca2+来诱导肠道分泌,然后Ca2+与钙调蛋白结合以刺激分泌过程。