The effect of bile acid on the activation of amiloride‐sensitive sodium channels in frog skin

The effect of bile acid on the activation of amiloride‐sensitive sodium channels in frog skin
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胆汁酸对青蛙皮肤阿米洛利敏感钠通道激活的影响

DOI:
10.1113/expphysiol.1996.sp003974
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发表时间:
1996
影响因子:
2.7
通讯作者:
KT Ferreira
KT Ferreira
中科院分区:
医学4区
文献类型:
--
作者:
M. Lima;H.C. Ferreira;KT Ferreira

文献摘要

被引文献

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在短路条件下,研究了胆汁酸--脱氧胆酸(DOC)对离体蛙皮运输性能的影响。在蛙皮顶侧加入DOC(1 Mm),可使短路电流(IAC)增加三倍。这种作用可被阿米洛利抑制。DOC还通过两种不同的机制增加了制剂的电导。在低浓度(<2.5 mM)时,它激活阿米洛利敏感的钠通道。在DOC浓度较高时,用22Na+、36Cl-测定的基侧-顶端单向通量。与[14C]菊粉相比,[14C]甘露醇和[14C]菊粉对Na+、Cl-和甘露醇的渗透性有选择性地增加。这些数据表明,钠离子和氯离子在整个制剂中使用相同的扩散途径。这一途径区分了氯化钠和甘露醇,并且对菊粉的区别更大。DOC对cAMP(1 MM)的影响是相加的。ADH(20mU·ml-1)、前列腺素E2(0.1微米)或Forsklin(10微米)。我们的研究表明,DOC刺激蛙皮肤ISC的最终作用是通过激活阿米洛利敏感的钠通道。然而,由于DOC是脂溶性的,不能排除直接激活腺苷环化酶或磷酸激酶A的可能性。
The effect of the bile acid, deoxycholic acid (DOC), on the transport properties of isolated frog skin was studied under short‐circuit conditions. The addition of DOC (1 mM) to the apical side of the frog skin induced a threefold increase in the short‐circuit current (Iac). This effect was inhibited by amiloride. DOC also increased the conductance of the preparation by two different mechanisms. At low concentrations (< 2.5 mM) it activated amiloride‐sensitive sodium channels. At higher concentrations of DOC, basolateral‐apical unindirectional fluxes, measured with 22Na+, 36Cl‐. [14C]mannitol and [14C]inulin, showed a selective increase in the permeability to Na+, Cl‐ and mannitol in relation to [14C]inulin. These data suggest that sodium and chloride ions use the same diffusional pathway across the preparation. This pathway discriminates between NaCl and mannitol, and discriminates even more in relation to inulin. The effects of DOC are additive to those of cAMP (1 mM). ADH (20 mU ml‐1), prostaglandin E2 (0.1 microM) or forskolin (10 microM). It is concluded from our study that the final effect of DOC in stimulating the Isc in frog skin is through the activation of amiloride‐sensitive sodium channels. However, since DOC is liposoluble, a direct activation of an adenylate cyclase or of phosphokinase A cannot be excluded.