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“The effect of nicotine exposure on surfactant gene expression is apparently mediated by nicotinic acetylcholine receptors because it was blocked by D-tubocurarine.”
The American journal of physiology • 1998 | View Paper
“4 Dihydro‐β‐erythroidine (DHBE) and tubocurarine antagonized both ACh and nicotine excitations but not those induced by glutamate or dl‐homocysteic acid.”
British journal of pharmacology • 1976 | View Paper
“T-REx293 cells expressed the nicotinic acetylcholine receptor (nAchR) and tubocurarine , an nAChR antagonist, completely blocked the effects of nicotine.”
The Journal of toxicological sciences • 2018 | View Paper
“The increased cell proliferation and gene upregulation induced by nicotine were inhibited by addition of the nicotinic receptor antagonist d-tubocurarine.”
Acta biochimica et biophysica Sinica • 2006 | View Paper
“Mecamylamine (10 μM), dihydro‐β‐erythroidine (10 μM) and d‐tubocurarine (30 μM), but not α‐bungarotoxin (α‐BTX, 0.1 μM), attenuated the NIC (100 μM)‐evoked release of [3H]‐NA.”
British journal of pharmacology • 2002 | View Paper
“In addition, we demonstrate direct cellular effects of nicotine on primary human bone cells and blockage of these effects with a nicotinic receptor antagonist, D-tubocurarine.”
Naunyn-Schmiedeberg's Archives of Pharmacology • 2001 | View Paper
“The increase in tau immunoreactivity induced by nicotine , epibatidine, and tacrine, but not the up‐regulation of nAChRs, was prevented by the antagonists d‐tubocurarine and mecamylamine.”
“The effect of nicotine on up-regulation of alpha7 AChRs was partially blocked by either d-tubocurarine or mecamylamine.”
“The effect of nicotine treatment on the number of alpha3 AChRs was only slightly blocked by the antagonists d-tubocurarine , mecamylamine, or dihydro-beta-erythroidine at concentrations that efficiently block alpha3 AChR function.”