Chen Y M, Dixon W R
Department of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence 66045.
Life Sci. 1990;46(16):1167-73. doi: 10.1016/0024-3205(90)90453-x.
The effect of etorphine on nicotine and muscarine-mediated catecholamine (CA) release from isolated perfused rat adrenal glands was investigated. Nicotine increased CA secretion at the low concentration of 0.5 micrograms while higher concentrations of muscarine (5 micrograms) were required. Moreover, muscarine released primarily epinephrine (EP) from rat adrenal glands while nicotine released norepinephrine (NE) and Ep. Etorphine inhibited NE and EP release evoked by nicotine to the same extent, whereas, muscarine-mediated release of NE and EP was not affected. Mecamylamine and verapamil inhibited nicotine but not muscarine-induced CA secretion. Our results suggest that etorphine preferentially interacts with nicotinic receptors on rat adrenal chromaffin cell membranes.
研究了埃托啡对尼古丁和毒蕈碱介导的从离体灌注大鼠肾上腺释放儿茶酚胺（CA）的影响。尼古丁在低浓度0.5微克时增加CA分泌，而毒蕈碱则需要更高浓度（5微克）。此外，毒蕈碱主要从大鼠肾上腺释放肾上腺素（EP），而尼古丁释放去甲肾上腺素（NE）和EP。埃托啡同等程度地抑制尼古丁诱发的NE和EP释放，而毒蕈碱介导的NE和EP释放不受影响。美加明和维拉帕米抑制尼古丁而非毒蕈碱诱导的CA分泌。我们的结果表明，埃托啡优先与大鼠肾上腺嗜铬细胞膜上的烟碱受体相互作用。
