Wöll E, Paulmichl M, Lang F, Glossmann H
Institute for Physiology, University of Innsbruck, Austria.
Eur J Pharmacol. 1991 Apr 3;195(3):399-401. doi: 10.1016/0014-2999(91)90482-6.
In Madin Darby canine kidney (MDCK) cells epinephrine--via alpha-adrenoceptors--leads to sustained hyperpolarization of the cell membrane. The present study defined the subtype of alpha-adrenoceptor involved. Both the alpha 1-adrenoceptor agonist, phenylephrine, and alpha 2-adrenoceptor agonists (BHT 920, guanfacine, moxonidine, oximetazoline) were able to hyperpolarize the cell membrane. The effect of epinephrine was only transient in the presence of the alpha 2-adrenoceptor antagonist, yohimbine, whereas the effect persisted in the presence of the alpha 1-adrenoceptor antagonist, prazosin. The epinephrine-induced hyperpolarization was almost abolished in the presence of both prazosin and yohimbine. In conclusion, both, alpha 1- and alpha 2-receptors are involved in the hyperpolarizing action of epinephrine.
在犬肾上皮细胞(MDCK)中,肾上腺素通过α-肾上腺素能受体导致细胞膜持续超极化。本研究确定了所涉及的α-肾上腺素能受体亚型。α1-肾上腺素能受体激动剂去氧肾上腺素和α2-肾上腺素能受体激动剂(BHT 920、胍法辛、莫索尼定、羟甲唑啉)均能使细胞膜超极化。在存在α2-肾上腺素能受体拮抗剂育亨宾的情况下,肾上腺素的作用只是短暂的,而在存在α1-肾上腺素能受体拮抗剂哌唑嗪的情况下,该作用持续存在。在同时存在哌唑嗪和育亨宾的情况下,肾上腺素诱导的超极化几乎被消除。总之,α1和α2受体均参与了肾上腺素的超极化作用。