The effect of secretagogues on ion conductances of in vitro perfused, isolated rabbit colonic crypts
The effect of secretagogues on ion conductances of in vitro perfused, isolated rabbit colonic crypts
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促分泌剂对体外灌注离体兔结肠隐窝离子电导的影响
DOI：
10.1007/bf00704154
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发表时间：
1995
期刊：
影响因子：
--
通讯作者：
R. Greger
中科院分区：
文献类型：
--
作者：
E. Lohrmann;R. Greger
本研究中使用了几种促分泌剂，包括增强细胞内环磷酸腺苷 (cAMP) 产生的促分泌剂，以及提高细胞内 Ca2+ 活性并已知可增加完整结肠和结肠癌细胞系中 Cl- 分泌的其他促分泌剂。检查它们对离体兔远端结肠隐窝电生理特性的影响。手动解剖隐窝并在体外灌注。估计跨上皮电压（Vte）、跨上皮电阻（Rte）、跨基底外侧膜的膜电压（Vbl）和分数基底外侧膜电阻（FRbl）。基底外侧前列腺素E2（PGE2，⩾0.1 μmol/l）、血管活性肠肽（VIP，1 nmol/l）和腺苷（0.1 mmol/l）诱导（Vbl）的初始去极化和继发部分复极化。在腺苷的情况下，(Vbl)的初始去极化为31±2mV(n=47)。Rte从16.4±3.6显着下降至14.2±3.7Ω·cm2(n=6)，FRb从0.11±0.02显着增加至0.51±0.10(n=6)。在第二阶段，复极(Vbl)达到11±2 mV (n=47)，达到-51±2 mV (n=47)的稳态(Vbl)。Rte进一步显着下降至稳态值12.4±3.8 Ω·cm2 (n=6)，FRbl显着下降至0.42±0.13 (n=6)。在 30% 的实验中，在腺苷洗出过程中观察到 (Vbl) 短暂超极化 8±2 mV (n=14)。在存在腺苷的情况下，但不在对照条件下，将管腔 Cl− 浓度从 120 降低至 32 mmol/l，去极化 (Vbl) 显着降低 8±1 mV (n=9)。基底外侧 ATP 和 ADP (0.1 mmol/l) 导致短暂的初始去极化，随后分别产生 6±2 mV (n=27) 和 5±4 mV (n=8) 的持续且显着的超极化。卡巴胆碱 (CCH) 以浓度依赖性方式超极化 (Vbl)。在 100 μmol/l（浴）时，超极化为 14±2 mV (n=11)，并且 FRbl 略有下降。神经降压素（⩾10 nmol/l）、异丙肾上腺素（⩾10 μmol/l）和尿苷5'-三磷酸（UTP，0.1 mmol/l）没有作用。结论是，PGE2、VIP 和腺苷通过增加细胞内 cAMP 浓度依次上调管腔 Cl− 电导和基底外侧 K+ 电导。 ATP、ADP 和 CCH 等 Ca2+ 动员激素会增加基底外侧 K+ 电导，而对管腔 Cl− 电导的影响似乎非常有限。
Several secretagogues were used in this study, including those which enhance intracellular cyclic adenosine monophosphate (cAMP) production, as well as others which elevate intracellular Ca2+ activity and are known to increase Cl− secretion in the intact colon and in colonic carcinoma cell lines. They were examined with respect to their effects on electrophysiological properties in isolated rabbit distal colonic crypts. Crypts were dissected manually and perfused in vitro. Transepithelial voltage (Vte), transepithelial resistance (Rte), membrane voltage across the basolateral membrane (Vbl), and fractional basolateral membrane resistance (FRbl), were estimated. Basolateral prostaglandin E2 (PGE2, ⩾0.1 μmol/l), vasoactive intestinal peptide (VIP, 1 nmol/l) and adenosine (0.1 mmol/l) induced an initial depolarisation and a secondary partial repolarisation of (Vbl). In the case of adenosine, the initial depolarization of (Vbl) was by 31±2 mV (n=47).Rte fell significantly from 16.4±3.6 to 14.2±3.7 Ω·cm2 (n= 6), andFRblincreased significantly from 0.11±0.02 to 0.51±0.10 (n=6). In the second phase the repolarisation of (Vbl) amounted 11±2 mV (n=47) and a steadystate (Vbl) of −51±2 mV (n=47) was reached.Rte fell further and significantly to a steady-state value of 12.4±3.8 Ω·cm2 (n=6) andFRbl fell significantly to 0.42±0.13 (n=6). In 30% of the experiments, a transient hyperpolarisation of (Vbl) by 8±2 mV (n=14) was seen during wash out of adenosine. In the presence of adenosine, but not under control conditions, lowering of luminal Cl− concentration from 120 to 32 mmol/l depolarised (Vbl) significantly by 8±1 mV (n=9). Basolateral ATP and ADP (0.1 mmol/l) led to a short initial depolarisation followed by a sustained and significant hyperpolarisation by 6±2 mV (n=27) and 5±4 mV (n=8), respectively. Carbachol (CCH) hyperpolarised (Vbl) in a concentration-dependent manner. At 100 μmol/l (bath) the hyperpolarisation was by 14±2 mV (n=11) andFRbl fell slightly. Neurotensin (⩾10 nmol/l), isoproterenol (⩾10 μmol/l) and uridine 5′-triphosphate (UTP, 0.1 mmol/l) had no effect. It is concluded that PGE2, VIP and adenosine upregulate sequentially a luminal Cl− conductance and a basolateral K+ conductance by increasing intracellular cAMP concentration. Ca2+ mobilising hormones such as ATP, ADP, and CCH increase the basolateral K+ conductance, while the effect on luminal Cl− conductance appears to be very limited.
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DOI：
10.1152/ajpgi.1986.250.2.g185
发表时间：
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期刊：
The American journal of physiology
影响因子：
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作者：
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DOI：
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发表时间：
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期刊：
The American journal of physiology
影响因子：
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作者：
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影响因子：
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DOI：
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发表时间：
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影响因子：
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作者：
Rogers,KV;Goldman,PS;Frizzell,RA;McKnight,GS
通讯作者：
McKnight,GS