首页> 外文期刊>The Journal of Physiology >Localization of cAMP- and aldosterone-induced K+ secretion in rat distal colon by conductance scanning.
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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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1. 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 (delta ISC) measurements. 2. Partial block of K+ absorption by mucosal ouabain did not change TEA-sensitive K+ secretion. Thus, K+ absorption and K+ secretion are not coupled. 3. Additivity of Rb+ fluxes as well as delta ISC 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. 4. 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 (delta ISC = 0.3 mumol h-1 cm-2), which increased during sham incubation. 5. Aldosterone (3 nM, 6 h in vitro incubation) resulted, after correction for the basal K+ secretion, in a K+ secretion of delta ISC = 0.9 mumol 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. 6. Adrenaline (5 microM) caused, in fresh tissue, a K+ secretion of delta ISC = 1.2 mumol 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). 7. 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:1.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 +净通量始终测量到使用短路电流(delta ISC)测量值变化估计的K +分泌量的80%。 2.粘膜哇巴因对K +的部分吸收没有改变TEA敏感的K +分泌。因此,K +吸收和K +分泌不耦合。 3.由3 nM醛固酮(体外孵育6小时)引起的Rb +流量以及δISC的可加性,随后,肾上腺素提示在存在阿米洛利的情况下醛固酮诱导的cAMP介导的K +分泌的可加性。 4.在对照条件下的电导扫描显示,表面上皮细胞中TEA敏感的K +电导率较小(0.3 +/- 0.2 mS cm-2),但隐窝中没有,并且表面上皮细胞中的基础K +分泌物较小(δISC = 0.3 mumol h-1 cm-2),在假孵育中会增加。 5.校正基础K +分泌后,醛固酮(3nM,体外温育6小时)导致δISC的K +分泌=0.9μmol·h-1cm-2。醛固酮在表面上皮细胞中诱导的TEA敏感电导率为1.1 +/- 0.3 mS cm-2,但在隐窝中却没有。 6.肾上腺素(5 microM)在新鲜组织中引起δISC的K +分泌= 1.2μmol·h-1 cm-2和隐窝(0.7 +/- 0.2 mS cm-2)和表面上皮细胞的电导率变化相等(0.7 +/- 0.1 mS cm-2)。 7.我们得出结论,醛固酮在生理浓度下诱导的K +分泌仅限于表面上皮,而cAMP介导的K +分泌在隐窝和表面上皮中均位于同一位置。

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