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氯化钡在大鼠结肠中的分泌作用。

The secretory action of barium chloride in rat colon.

作者信息

Hardcastle J, Hardcastle P T, Noble J M

出版信息

J Physiol. 1985 Apr;361:19-33. doi: 10.1113/jphysiol.1985.sp015630.

DOI:10.1113/jphysiol.1985.sp015630
PMID:3989726
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1192844/
Abstract

BaCl2, applied serosally, caused a rise in the p.d. and short-circuit current (s.c.c), and a decrease in tissue resistance in stripped sheets of rat colon. This response was dose dependent. Mucosal application of BaCl2 was without effect. The BaCl2-induced rise in s.c.c. was inhibited by reducing the serosal Na+ concentration to 25 mM. Lowering the mucosal Na+ concentration was without effect. Ouabain (10(-3) M in serosal fluid) and furosemide (10(-3) M in serosal fluid) both reduced the rise in s.c.c. induced by BaCl2. Flux determinations indicated that BaCl2 inhibited Na+ absorption and stimulated Cl- secretion by the colon. In vivo, BaCl2 increased fluid accumulation within the colonic lumen, an effect that was associated with a rise in the transcolonic p.d. Increasing the serosal K+ concentration to 20 mM reduced the responses to BaCl2, acetylcholine and theophylline, and this could not be entirely accounted for by the concomitant reduction in the serosal Na+ concentration. As high serosal K+ did not mimic the secretory response it would appear that BaCl2 does not act by blocking K+ channels. The rise in s.c.c. induced by BaCl2 was not reduced by Ca2+-free conditions, but it was inhibited by 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride (TMB-8) and trifluoperazine. BaCl2 did not alter cyclic AMP production by colonic scrapes. It is concluded that BaCl2 induces colonic secretion by the release of intracellular Ca2+, which then combines with calmodulin to activate the secretory process.

摘要

经浆膜面施加的氯化钡可使大鼠结肠剥脱片的跨膜电位(p.d.)和短路电流(s.c.c)升高,组织电阻降低。这种反应呈剂量依赖性。经黏膜面施加氯化钡则无作用。将浆膜面钠离子浓度降至25 mM可抑制氯化钡诱导的短路电流升高。降低黏膜面钠离子浓度则无作用。哇巴因(浆膜液中浓度为10⁻³ M)和呋塞米(浆膜液中浓度为10⁻³ M)均可降低氯化钡诱导的短路电流升高。通量测定表明,氯化钡抑制结肠对钠离子的吸收并刺激氯离子分泌。在体内,氯化钡增加结肠腔内的液体蓄积,这一效应与跨结肠跨膜电位升高相关。将浆膜面钾离子浓度增至20 mM可降低对氯化钡、乙酰胆碱和茶碱的反应,且这不能完全由同时降低的浆膜面钠离子浓度来解释。由于高浓度浆膜面钾离子并未模拟分泌反应,因此氯化钡似乎并非通过阻断钾离子通道起作用。无钙条件下,氯化钡诱导的短路电流升高未降低,但可被盐酸8-(N,N-二乙氨基)辛基-3,4,5-三甲氧基苯甲酸酯(TMB-8)和三氟拉嗪抑制。氯化钡未改变结肠刮片的环磷酸腺苷生成。结论是,氯化钡通过释放细胞内钙离子诱导结肠分泌,然后钙离子与钙调蛋白结合以激活分泌过程。

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本文引用的文献

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