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Localization of cAMP- and aldosterone-induced K+ secretion in rat distal colon by conductance scanning

机译:电导扫描在大鼠远端结肠中定位cAMP和醛固酮诱导的K +分泌

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摘要

Aldosterone- and adrenaline-induced K+ secretion were investigated in rat late distal colon using conductance scanning and Ussing chamber techniques. K+ secretion was unmasked by the K+ channel blocker tetraethylammonium (TEA). Electrogenic Na+ absorption was inhibited by amiloride. Rb+ net fluxes consistently measured about 80 % of K+ secretion estimated using change in short-circuit current (ΔISC) measurements.Partial block of K+ absorption by mucosal ouabain did not change TEA-sensitive K+ secretion. Thus, K+ absorption and K+ secretion are not coupled.Additivity of Rb+ fluxes as well as ΔISC caused by 3 nM aldosterone (6 h in vitro incubation) and, subsequently, adrenaline suggested additivity of aldosterone-induced and cAMP-mediated K+ secretion in the presence of amiloride.Conductance scanning under control conditions revealed a small TEA-sensitive K+ conductivity in surface epithelium (0.3 ± 0.2 mS cm−2) but not in crypts, as well as a small basal K+ secretion in surface epithelium (ΔISC = 0.3 μmol h−1 cm−2), which increased during sham incubation.Aldosterone (3 nM, 6 h in vitro incubation) resulted, after correction for the basal K+ secretion, in a K+ secretion of ΔISC = 0.9 μmol h−1 cm−2. Aldosterone induced a TEA-sensitive conductivity of 1.1 ± 0.3 mS cm−2 in surface epithelium, but not in crypts.Adrenaline (5 μm) caused, in fresh tissue, a K+ secretion of ΔISC = 1.2 μmol h−1 cm−2 and equal conductivity changes in crypts (0.7 ± 0.2 mS cm−2) and surface epithelium (0.7 ± 0.1 mS cm−2).We conclude that K+ secretion induced by aldosterone in physiological concentration is restricted to surface epithelium, whereas cAMP-mediated K+ secretion is located equally in crypts and surface epithelium.
机译:使用电导扫描和Ussing chamber技术研究了大鼠晚期远端结肠中醛固酮和肾上腺素诱导的K +分泌。 K +通道阻滞剂四乙铵(TEA)不能掩盖K +分泌。阿米洛利可抑制电致钠离子的吸收。 Rb +净通量始终测量到约80%的K +分泌量,这是通过短路电流(ΔISC)测量的变化估算得出的。粘膜哇巴因对K +的部分吸收不会改变TEA敏感的K +分泌。因此,Kn的吸收和K +的分泌没有耦合.3 nM醛固酮(体外培养6 h)引起的Rb +流量和ΔISC的加性,随后肾上腺素提示醛固酮诱导和cAMP介导的K +分泌的可加性。对照条件下的电导扫描显示表面上皮(0.3±0.2 mS cm-2)中有少量TEA敏感的K +电导率,但隐窝中无,以及表面上皮中有少量基础K +分泌(ΔISC= 0.3μmol h−1 cm−2)在假孵育中增加。醛固酮(3 nM,体外孵育6 h)在校正基础K +分泌后导致ΔISC= 0.9μmolh-1 cm-2的K +分泌。 。醛固酮在表面上皮细胞中引起的TEA敏感电导率为1.1±0.3 mS cm-2,但在隐窝中却没有。肾上腺素(5μm)在新鲜组织中引起K +分泌ΔISC= 1.2μmolh-1 cm-2和隐窝(0.7±0.2 mS cm-2)和表面上皮细胞(0.7±0.1 mS cm-2)的电导率变化相等。我们得出结论,在生理浓度下醛固酮诱导的K +分泌仅限于表面上皮,而cAMP介导的K +分泌位于隐窝和表面上皮中。

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