首页> 美国卫生研究院文献>The Journal of Physiology >Pancreatic acinar cells: effect of acetylcholine pancreozymin gastrin and secretin on membrane potential and resistance in vivo and in vitro.
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Pancreatic acinar cells: effect of acetylcholine pancreozymin gastrin and secretin on membrane potential and resistance in vivo and in vitro.

机译:胰腺腺泡细胞:乙酰胆碱胰酶胃泌素和促胰液素在体内外对膜电位和抗性的影响。

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摘要

1. Intracellular recordings of membrane potential and input resistance have been made in vivo and in vitro from the exocrine acinar cells of rat pancreas using indwelling glass micro-electrodes. 2. The resting cell membrane potential and input resistance in the in vivo experiments were not markedly different from the values obtained in the in vitro experiments. The effect of both acetylcholine (ACh) and pancreozymin (CCK-Pz) on the pancreas in vivo as well as in vitro was to reduce both the acinar cell membrane potential and the input resistance narkedly. The amplitude of the evoked depolarization and the change in input resistance evoked by supramaximal stimuli were of the same magnitude in both types of preparations. 3. Gastrin had an effect on the acinar cell potential and resistance which was indistinguishable from that of CCK-Pz or ACh. The effect of gastrin or CCK-Pz was, in contrast to that of ACh, not influenced by the presence of atropine. The reversal potential for the gastrin evoked potential change was about -20 mV. 4. Secretin in doses producing maximal volume secretion in vivo had no effect on acinar cell membrane potential and input resistance. 5. Dibutyryl cyclic AMP (5mM) and cyclic GMP (1mM) had no effect on cell membrane potential or resistance. 6. It is concluded that the in vitro superfused pancreas segment preparation is a useful model system in electrophysiological studies since it functions essentially as the in vivo preparation. In contrast to both gastrin and CCK-Pz, secretin has no effect on the bioelectrical properties of the acinar cells, indicating that there are no physiologically important secretin receptors in rat acinar cells.
机译:1.使用留置玻璃微电极从大鼠胰腺的外分泌腺泡细胞体内和体外进行膜电位和输入阻力的细胞内记录。 2.体内实验中的静止细胞膜电位和输入阻力与体外实验中获得的值没有显着差异。乙酰胆碱(ACh)和胰酶(CCK-Pz)在体内和体外对胰腺的作用都是降低腺泡细胞膜电位和降低输入阻抗。在两种类型的制剂中,诱发的去极化幅度和超最大刺激引起的输入电阻变化幅度相同。 3.胃泌素对腺泡细胞的电位和抵抗力的影响与CCK-Pz或ACh的影响没有区别。与ACh相比,胃泌素或CCK-Pz的作用不受阿托品的存在影响。胃泌素引起的电位改变的反向电位约为-20mV。 4.促胰液素在体内产生最大体积分泌的剂量对腺泡细胞膜电位和输入阻力没有影响。 5.二丁酰基环状AMP(5mM)和环状GMP(1mM)对细胞膜电位或抗性没有影响。 6.结论是,体外超融合胰腺片段制剂在电生理研究中是有用的模型系统,因为它基本上起着体内制剂的作用。与胃泌素和CCK-Pz相比,促胰液素对腺泡细胞的生物电特性没有影响,这表明大鼠腺泡细胞中没有生理上重要的促胰液素受体。

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