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蛙皮上皮细胞中钾离子刺激的钠离子转运

K+ -stimulated Na+ transport in frog-skin epithelia.

作者信息

Kaufman A I, Erlij D

出版信息

Pflugers Arch. 1986 Dec;407(6):596-601. doi: 10.1007/BF00582637.

Abstract

Increasing [K+] from 2.5 mmol/l to 115 mmol/l on the serosal side of the frog skin produces a rapid decrease of short-circuit current (Isc) that is followed, within a few minutes, by a recovery of Isc to near or above its control value. After isolation of the epithelium by a procedure involving collagenase treatment and physical removal of the corium, increasing serosal [K+] still produced a depression of Isc but no significant recovery phase. By itself, collagenase treatment reduced but did not eliminate the recovery phase. The recovery phase was also markedly depressed by the beta-adrenergic blocker oxprenolol, but not by propranolol, atropine or indomethacin. Amiloride, given during the recovery phase, caused Isc to reverse to a small outward value. These results suggest that the recovery phase of Isc seen in the response to increased serosal [K+] represents an increase in Na+ influx through amiloride-sensitive channels which is triggered by the release of an intermediary agent, possibly a beta-adrenergic agonist, from some structure in the corium.

摘要

将蛙皮浆膜侧的[K⁺]从2.5 mmol/L提高到115 mmol/L会使短路电流(Isc)迅速降低,几分钟内Isc又会恢复到接近或高于其对照值。通过胶原酶处理和物理去除真皮的方法分离上皮后,提高浆膜[K⁺]仍会使Isc降低,但无明显的恢复阶段。单独的胶原酶处理会减少但不会消除恢复阶段。β-肾上腺素能阻滞剂氧烯洛尔会显著抑制恢复阶段,但普萘洛尔、阿托品或吲哚美辛则不会。在恢复阶段给予氨氯吡咪会使Isc反向变为一个小的外向值。这些结果表明,对浆膜[K⁺]升高的反应中所见的Isc恢复阶段代表通过氨氯吡咪敏感通道的Na⁺内流增加,这是由真皮中某种结构释放的一种中间介质(可能是β-肾上腺素能激动剂)触发的。

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