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1 specific beta3 antagonist), propranolol, and bethanechol.
2 ates following intravenous administration of bethanechol, a cholinergic agonist, or intralumenal inst
7 ed gastric relaxation was enhanced following bethanechol and reduced by l-NAME administration, sugges
9 esponse to direct cholinergic stimulation by bethanechol at 2 days postsympathectomy were increased f
10 e effects of SScIgGs on M(3)-R activation by bethanechol (BeCh), M(3)-R occupancy, and receptor bindi
11 ing doses of the muscarinic receptor agonist bethanechol, but not the nicotinic receptor antagonist m
12 ent with the pro-motility muscarinic agonist bethanechol, but were abolished by systemic administrati
14 ximal fluorescence loss, however, required a bethanechol concentration three times greater than that
17 m allografts only generated 23% of the total bethanechol-induced contractile force in vitro compared
18 reatic beta-cells with a muscarinic agonist (bethanechol) led to significantly increased plasma insul
21 d in UP-LPS-treated TLR4-competent mice, but bethanechol-stimulated contractions were not altered by
24 nt 2-deoxy-D-glucose (75 mg kg(-1)), whereas bethanechol-stimulated pancreatic protein output was inh
26 e pronounced when lungs were also exposed to bethanechol to stimulate submucosal gland secretion, whe
29 l muscle contractions caused by nicotine and bethanechol were similar in segments from P2X2+/+ and P2
30 l muscle contractions caused by nicotine and bethanechol were similar in segments from P2X3+/+ and P2