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1 ropic response to the acetylcholine analogue carbamylcholine.
2 ilrinone nor H-89 changed the HR response to carbamylcholine.
3 ptor is blocked by alpha-bungarotoxin and by carbamylcholine.
4  to controls and a loss of responsiveness to carbamylcholine.
5 renol and the muscarinic cholinergic agonist carbamylcholine.
6 K1 with either the chick M2 or M4 mAChR gave carbamylcholine (10 microm)-stimulated K+ currents of 30
7 lation but not to the acetylcholine analogue carbamylcholine (100 nM).
8 tinic agonists acetylcholine (1-100 microM), carbamylcholine (3-100 microM), or nicotine (3-10 microM
9                 Whereas the flexible agonist carbamylcholine (5 microM) was shown to induce channels
10 r-228 with [(14)C]halothane was increased by carbamylcholine (90%) or d-tubocurarine (50%), but it wa
11 ells, incubation with a cholinergic agonist (carbamylcholine), a regulatory peptide (cholecystokinin)
12 ations were challenged with the secretagogue carbamylcholine, a subpopulation of zymogen granules bec
13          Wild-type alphadelta complexes bind carbamylcholine about 30-fold more tightly than alphagam
14 ows an additivity in free energy changes for carbamylcholine and d-tubocurarine, suggesting independe
15 rystal structures of AChBP in complexes with carbamylcholine and nicotine reveal the basis for agonis
16         The anti-fibrillatory action of both carbamylcholine and sodium nitroprusside was ultimately
17                                 the agonists carbamylcholine and tetramethylammonium also activate th
18 eral mutated, receptors using acetylcholine, carbamylcholine and tetramethylammonium as agonists.
19 their epitopes and their effects on agonist (carbamylcholine) and antagonist [alpha-bungarotoxin (alp
20 lcium as a second messenger (e.g., cerulein, carbamylcholine, and bombesin) but not to those that use
21 d with the agonists nicotine, acetylcholine, carbamylcholine, and epibatidine.
22 ments on embryonic wild-type receptors using carbamylcholine as an agonist with low efficacy.
23 alpha subunit in 293 HEK cells, and measured carbamylcholine binding affinity of intracellular comple
24   The present study compares epibatidine and carbamylcholine binding in terms of their site and state
25 form the desensitized state of the receptor, carbamylcholine binding was measured in the presence of
26  establish that, in the presence of agonist (carbamylcholine), both drugs photolabeled amino acids on
27 TCP and [(3)H]imipramine to the desensitized/carbamylcholine-bound Torpedo AChR with higher affinity
28  0.9 k(B)T more binding energy per site than carbamylcholine but approximately 3.1 k(B)T more than ch
29           Chronic treatment with nicotine or carbamylcholine, but not d-tubocurarine, mecamylamine, o
30 tion of beat rate by the muscarinic agonist, carbamylcholine, by 5-fold and decreased expression of G
31 t with forskolin but only in the presence of carbamylcholine (carbachol).
32                            cGMP responses to carbamylcholine (CCh) (stimulated, basal) and sodium nit
33                     When coapplied with 1 mM carbamylcholine (CCh), TEA decreased the effective openi
34 tenuation of ICa-L by the muscarinic agonist carbamylcholine (CCh).
35 viously attenuated by the muscarinic agonist carbamylcholine (CCh, 1 mumol/L), SIN-1 had no additive
36                                              Carbamylcholine (CCh, 200 nmol l(-1) , n = 9) significan
37 ase in the negative chronotropic response to carbamylcholine characterized by a 2.4-fold decrease in
38 l/l glucose, the muscarinic receptor agonist carbamylcholine chloride (CCh) evoked a concentration-de
39 s to the bath-applied acetylcholine analogue carbamylcholine chloride in +EX and -EX atria (IC(50) co
40  was affected by the presence of the agonist carbamylcholine, consistent with photoincorporation at t
41          Conversely, the cholinergic agonist carbamylcholine decreased I(M) in the presence of SR1417
42 havior, and that isoproterenol increased and carbamylcholine decreased the beating rate in both hESC-
43 e same refinement procedure to the data from carbamylcholine desensitized AChR we find 18 fewer Tb3+
44 und receptor, neither of the two subunits in carbamylcholine-desensitized receptor, and to both alpha
45 in the closed resting state with that in the carbamylcholine-desensitized state.
46 tween genotypes, but the cholinergic agonist carbamylcholine enhanced glucose-induced insulin secreti
47 e site selectivities between epibatidine and carbamylcholine; for epibatidine the rank order of affin
48                                              Carbamylcholine increased NO metabolite content in the c
49  or alpha3 beta2 alpha5 AChRs to nicotine or carbamylcholine increased their amount up to 24-fold but
50  that XeC selectively blocks bradykinin- and carbamylcholine-induced Ca2+ efflux from endoplasmic ret
51 trial cells 5 days in ovo, TGFbeta increased carbamylcholine inhibition of beat rate 2.5-fold and inc
52 hese data demonstrate a protective effect of carbamylcholine on VFT that depends upon both muscarinic
53 y d-tubocurarine, whereas addition of either carbamylcholine or isoflurane had no effect.
54 holine receptors activated by acetylcholine, carbamylcholine, or choline.
55 gated with additional agonists (nicotine and carbamylcholine), partial agonists (lobeline and 4-hydro
56 art, we show that the acetylcholine analogue carbamylcholine raises ventricular fibrillation threshol
57                  In contrast to epibatidine, carbamylcholine shows little site selectivity for desens
58 om Akita mice exhibited a markedly decreased carbamylcholine stimulation of I(KAch) with a peak value
59 silon > alphagamma > alphadelta, whereas for carbamylcholine the rank order is alphadelta congruent w
60 nt of 100 nM; in the presence of the agonist carbamylcholine this value decreased to 10 nM.
61  monitor the current fluctuations induced by carbamylcholine upon the insertion into the plasma membr
62              The anti-fibrillatory action of carbamylcholine was prevented by the nicotinic receptor

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