Krippeit-Drews P, Welker S, Drews G
Institute of Pharmacy, University of Tübingen, Germany.
Biochem Biophys Res Commun. 1996 Jul 5;224(1):199-205. doi: 10.1006/bbrc.1996.1007.
The effects of the nitric oxide (NO) synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) were studied on electrical activity, K+ATP currents and voltage-dependent K+ and Ca2+ channel currents in mouse pancreatic B cells. In the presence of 15 mM glucose, L-NAME (> 5 mM) depolarized the B cell membrane and electrical activity became continuous. The depolarization caused by L-NAME was not reversed by the addition of a membrane permeant cyclic GMP analogue. L-NAME inhibited the whole-cell K+ATP current reversibly by reducing the single channel current conductance and open probability. The results are consistent with the assumption that L-NAME depolarizes the B cell membrane by a direct action on the K+ATP channel. L-NAME also influenced the whole-cell current through voltage-dependent K+ and Ca2+ channels.
研究了一氧化氮(NO)合酶抑制剂Nω-硝基-L-精氨酸甲酯(L-NAME)对小鼠胰腺β细胞电活动、K+ATP电流以及电压依赖性K+和Ca2+通道电流的影响。在15 mM葡萄糖存在的情况下,L-NAME(> 5 mM)使β细胞膜去极化,电活动变得持续。L-NAME引起的去极化不会因添加膜通透性环鸟苷酸类似物而逆转。L-NAME通过降低单通道电流电导和开放概率可逆地抑制全细胞K+ATP电流。这些结果与L-NAME通过直接作用于K+ATP通道使β细胞膜去极化的假设一致。L-NAME还通过电压依赖性K+和Ca2+通道影响全细胞电流。