ライフサイエンスコーパス: carbachol

1 e, high-K+ depolarization) and/or [Ca2+]cyt (carbachol).

2 usiform cells using the cholinergic agonist, carbachol.

3 nsitivity to AF induction in the presence of carbachol.

4 tor protein CPI-17 were also stimulated with carbachol.

5 y in the presence of the orthosteric agonist carbachol.

6 scle cells induced by the muscarinic agonist carbachol.

7 vity of beta-cells to the cholinergic analog carbachol.

8 tractile responses to the muscarinic agonist carbachol.

9 n was slower for acetylcholine than that for carbachol.

10 ged for acetylcholine compared with that for carbachol.

11 roreflex and chemoreflex stimulation or with carbachol.

12 ed by application of the cholinergic agonist carbachol.

13 ed with forskolin and a low concentration of carbachol.

14 ess in response to all other agonists except carbachol.

15 fected by cholinergic receptor activation by carbachol.

16 cAMP-independent agonist cholinergic agonist carbachol.

17 zation or in response to M3 receptor agonist Carbachol.

18 substantially reduced, but usually less than carbachol.

19 myocytes treated with the muscarinic agonist carbachol.

20 d in the presence of the muscarinic agonist, carbachol.

21 ite the continued perfusions of the STN with carbachol.

22 r isoproterenol but not increases induced by carbachol.

23 ogical treatment with the muscarinic agonist carbachol.

24 l as MCCV increases produced by forskolin or carbachol.

25 very or prevented inhibition if added before carbachol.

26 or closely related synthetic analogs such as carbachol.

27 d does not support the inhibition of NHE3 by carbachol.

28 f cooperativity with the orthosteric agonist carbachol.

29 uired for the inhibition of NHE3 activity by carbachol.

30 o the plasma membrane after stimulation with carbachol.

31 ronotropic effects of the muscarinic agonist carbachol.

32 of oxygen saturation, and responsiveness to carbachol.

33 10 muM) and by the Ca(2+)-elevating agonist, carbachol (0.3 muM).

34 dialysis of the cholinergic receptor agonist carbachol (1 mM) into the STN caused an increase in the

35 a change from physiologic concentrations of carbachol (1 muM) to a supraphysiologic concentration (1

36 Following TTX application, carbachol (1 muM), substance P (1 muM) and an NKI agonis

37 , and stimulated with the muscarinic agonist carbachol (1 muM).

38 the LH and the RVM, the cholinergic agonist carbachol (125 nmol) was microinjected into the LH of fe

39 brief application of the cholinergic agonist carbachol (25 microM) or elevated KCl in glucose-contain

40 ations throughout TM3 on the interactions of carbachol, 4-n-butyl-1-[4-(2-methylphenyl)-4-oxo-1-butyl

41 Using local photolysis of caged carbachol, a broad-spectrum cholinergic agonist, we mapp

42 al signal of taste novelty, in these studies carbachol, a direct cholinergic agonist, was infused int

43 Treatment of H508 cells with carbachol, a hydrolytically stable acetylcholine analog,

44 Carbachol, a known nAChR and muscarinic receptor agonist

45 ith type 3 muscarinic receptor (M3), we used carbachol, a ligand specific for muscarinic receptor, as

46 ty between BQCA and the orthosteric agonist, carbachol, across pathways.

47 Carbachol acted presynaptically by increasing the freque

48 o not alter its sensitivity to inhibition by carbachol acting through the Galphaq-11-PLCbeta signalin

49 The muscarinic receptor agonist carbachol activated ERK1/2 better in T1R3-depleted cells

50 Carbachol-activated TRPC5 currents were recorded by the

51 nstrate that the muscarinic receptor agonist carbachol activates AMPKalpha1-containing complexes in t

52 Adding carbachol after isoproterenol caused dissociated antegra

53 se display loss of potency for acetylcholine/carbachol alongside a concurrent gain in potency for the

54 Carbachol also increased the frequency of spontaneous ex

55 Co-stimulation with carbachol and 8-pCPT-2'-O-Me-cAMP led to an additive eff

56 M2R-IKACh signaling pathway in SAN cells to carbachol and a significant slowing of M2R-IKACh deactiv

57 ted in the RVM following LH stimulation with carbachol and abolished LH-induced antinociception as we

58 after stimulating muscarinic receptors with carbachol and after stimulating purinergic receptors wit

59 nse to common pharmacological agents such as carbachol and atropine but rarely form capillary-like st

60 entiated by isoproterenol and abolished with carbachol and AVRs had abundant sympathetic nerve ending

61 The increase in [Ca2+]i caused by carbachol and BzATP used simultaneously was less than ad

62 mucosa inhibited ion transport responses to carbachol and forskolin but potentiated the reduced ion

63 ssue was tested for contractile responses to carbachol and histamine.

64 In isolated islets, carbachol and PACAP/VIP synergistically promote beta-cel

65 The effects of high glucose on reactivity to carbachol and phenylephrine were determined.

66 gill retina with acetylcholine or its analog carbachol and that these agents act through muscarinic r

67 o increase respiration in response to small (carbachol) and moderate (K(+) -depolarization) workloads

68 Secretagogues (cerulein, carbachol, and bombesin) can induce protease activation

69 CCK-8, carbachol, and bombesin, but not VIP/secretin, decreased

70 th IL-13 increased the potency of histamine, carbachol, and leukotriene D(4) as contractile agonists.

71 holine receptor activation by acetylcholine, carbachol, and other muscarinic agonists.

72 y of the full agonists, acetylcholine (ACh), carbachol, and oxotremorine-M, while significantly incre

73 the cholinergic agonists, acetylcholine and carbachol, and the cholinergic antagonists, D-tubocurari

74 Stimulation with cholecystokinin (CCK), carbachol, and vasoactive intestinal peptide all induced

75 on of NO-dependent signalling prevented both carbachol- and activity (5 Hz)-dependent LTD but not act

76 ne exemplified by orthosteric compounds like carbachol, another by structural analogs of AC-42, and a

77 Carbachol application had heterogeneous effects on neuro

78 SR-driven excitatory events was augmented by carbachol application.

79 exhibited a reduction in selectivity during carbachol application.

80 By injecting carbachol at the beginning of the light period or beginn

81 tractile or RLC phosphorylation responses to carbachol between tissues from normal mice vs. MYPT1 T85

82 All mutations tested severely reduced carbachol binding and activation of M(1).

83 n constants of 6 and 26 mM were obtained for carbachol binding to the A- and P-sites in E and of 2 an

84 e A- and P-sites in E and of 2 and 32 mM for carbachol binding to the A- and P-sites in EC.

85 Familiar taste-illness pairing following carbachol, but not vehicle, induced significant elevatio

86 phospholipase C inhibitor U-73122 abolished carbachol- but not forskolin-induced Rap1 activation.

87 3% showed evidence of a decreased potency of carbachol by a shift in the dose-response curve to the r

88 C6 glioma cells without altering TRAP-6 and carbachol Ca(2+) responses.

89 ivity-specifically, elevated Ca(2+) related (carbachol/Ca(2+) ionophore), but there was normal inhibi

90 ne microinjections of a cholinergic agonist, carbachol, can repeatedly elicit REM sleep-like episodes

91 The mixed muscarinic agonist carbachol (CAR) hyperpolarized all type II (A current) P

92 Here, we focus on the reaction of carbachol (carbamoylcholine) with AChE.

93 pressing M1 receptors, a muscarinic agonist (carbachol) causes a 40% decrease of F(surf) in normal me

94 ate (KA, 200 nm) and the cholinergic agonist carbachol (Cb, 10 mum) fast network oscillations, in the

95 hologic responses to the cholinergic agonist carbachol (Cch) and cholecystokinin (CCK-8), including 1

96 n increased maximal contractions (E(max)) to carbachol (CCh) and KCl.

97 nar cell responses to the muscarinic agonist carbachol (CCh) and the bile acid taurolithocholic acid

98 scarinic acetylcholine receptor, the agonist carbachol (Cch) caused strong activation of CFTR through

99 ulation; 3-4 muM L-glutamate (Glu) and 3 muM carbachol (CCh) evoked rapid Ca(2+) transients only in n

100 Importantly, the cholinergic agonist carbachol (CCh) induces gamma oscillations in vitro, via

101 ic fundus muscles stimulated by bath-applied carbachol (CCh) or cholinergic motor neurotransmission.

102 ter stimulation with the cholinergic agonist carbachol (Cch) or epidermal growth factor (EGF) for 5 m

103 The cholinergic agonist carbachol (Cch) stimulated the secretion of lacritin and

104 Carbachol (CCh) stimulation of HEK293 cells expressing w

105 epression), cholinergic agonist (5-10 microM carbachol (CCh)) reduced the amplitude of the first EPSP

106 We report that bath application of 3 mum carbachol (CCh), a muscarinic acetylcholine receptor ago

107 Carbachol (CCh), a muscarinic receptor-specific agonist,

108 muscarinic agonists oxotremorin-M (Oxo-M) or carbachol (CCh), although all three ligands have similar

109 Stimulation of isolated acinar cells with carbachol (CCh), histamine or ATP was associated with ma

110 Chronic application of the mAchR agonist, carbachol (Cch), induces Arc transcription via ERK signa

111 ined the contributions of Orai1 and TRPC1 to carbachol (CCh)-induced [Ca(2+)](i) signals and activati

112 hronic exposure to 10 mM histamine inhibited carbachol (CCh)-induced beta-hexosaminidase secretion an

113 he submucosal plexus) of rat proximal colon, carbachol (CCh)-induced Cl(-) secretion was decreased by

114 Carbachol (CCh)-mediated contraction was increased in bl

115 t on theta-frequency IPSC rhythms induced by carbachol (CCh).

116 ntrained by pulses of a cholinergic agonist, carbachol (CCh).

117 ore stimulation with the cholinergic agonist carbachol (Cch, 10(-4) M) for 5 minutes.

118 Carbachol (CCh, 100 nm and 1 mum) induced a sustained in

119 Protein secretion was induced by lacritin or carbachol (Cch, positive control).

120 maintained during a progressive decrease of carbachol concentration, even down to concentrations tha

121 shortening during a progressive decrease of carbachol concentration.

122 Carbachol concentration/temporal-force responses were si

123 tion was strongly potentiated by low VIP and carbachol concentrations that individually were unable t

124 We then show that carbachol consistently depresses this input and that thi

125 By contrast, carbachol delivery to parietal cortex, or noradrenaline

126 at observed during wakefulness induced after carbachol delivery to PFC.

127 s not restored during wakefulness induced by carbachol delivery to PFC.

128 We recently demonstrated that carbachol delivery to prefrontal cortex (PFC) restored w

129 Concentration/temporal responses to carbachol demonstrated similar sensitivities for bovine

130 The local photolysis of caged carbachol demonstrated that the functional expression of

131 Concentration/temporal responses to carbachol demonstrated tight coupling between force deve

132 ic receptor stimulation with the addition of carbachol, demonstrating "accentuated antagonism." Okada

133 The synchronizing action of carbachol depended on the glucose concentration used, su

134 treatment reversed these impairments whereas carbachol did not.

135 Additionally, carbachol directly affects HMNs by a variable combinatio

136 We also found that carbachol directly excited SLDsp neurons by activating a

137 reviously exposed to the cholinergic agonist carbachol, displayed longer neurites.

138 Furthermore, glucose and carbachol do not significantly affect Kv2.1 inactivation

139 toma cells, whereas the nonmitogenic agonist carbachol does not.

140 was possible to characterize the potency of carbachol (EC50=10.5 microM) and pirenzepine (IC50=4.2 m

141 The carbachol effect was blocked by atropine and SLM-driven

142 BIM I) produced the same enhancing effect on carbachol-evoked calcium mobilization as overexpressed D

143 th phorbol 12-myristate 13-acetate shortened carbachol-evoked calcium responses and occluded the effe

144 l) from patients with primary SS reduced the carbachol-evoked increase in [Ca2+]i in both mouse and h

145 -specific inactivation of ATG5 did not alter carbachol-evoked saliva and amylase secretion.

146 with nanosensors and their responsiveness to carbachol-evoked store release ( 400 nM).

147 ris propria developed tension in response to carbachol ex vivo and that mucosa demonstrated squamous

148 timulated only with a Ca2+-mediated agonist (carbachol), exocytosis was followed by poor discharge as

149 soproterenol compared with controls, whereas carbachol failed to inhibit isoproterenol-stimulated NCX

150 Cells were also exposed to VIP, carbachol, forskolin, and/or 3-isobutyl-1-methylxanthine

151 n of TRPC1 protein by either thapsigargin or carbachol further protected SH-SY5Y cells from salsolino

152 In both exposed and control animals, 100 muM carbachol had a transient excitatory effect on spontaneo

153 proved DMTP, whereas the cholinergic agonist carbachol impaired performance at the highest dose teste

154 r (FLIPR) functional assay (EC50, 36 nM) and carbachol in a hippocampal slice electrophysiology assay

155 pendent Isc was also produced by basolateral carbachol in all preparations except rabbit and the H441

156 The effect of carbachol in astrocytes was due to the activation of M3

157 t promoted by the muscarinic receptor ligand carbachol in freshly dispersed rat parotid acinar cells.

158 receptor currents by the muscarinic agonist carbachol in hippocampal pyramidal cells.

159 cally exaggerated bradycardia in response to carbachol in mice and isolated perfused hearts and signi

160 agonist reverted the stimulatory effects of carbachol in naive mice to levels comparable with those

161 rmation stimulated by norepinephrine but not carbachol in transfected HEK293 cells.

162 skolin together is synergistic; both VIP and carbachol increase intracellular [Ca2+] in SLHMG cells;

163 Carbachol increased ATP release from lacrimal gland piec

164 l effects on ICC-IM, whereas neostigmine and carbachol increased Ca(2+) transients.

165 Exposure of astrocytes to carbachol increased the expression of the extracellular

166 olinergic receptors with bath application of carbachol increased the firing rate of large (>20 mum di

167 Carbachol increased the phosphorylation of Pyk2 on tyros

168 Carbachol increased the probability of SR input to drive

169 As predicted from functional studies, carbachol increases F(surf) when cytoplasmic Ca(2) is in

170 stimulated by veratridine, but not by KCl or carbachol, indicating that the Ca2+ uniporter pathway pl

171 Fourth, carbachol induced a rapid and transient increase in endo

172 At the cellular level, carbachol induced an increase in the intracellular [Ca(2

173 The muscarinic agonist carbachol induced pronounced transient PKCbetaI transloc

174 Ethanol caused a doubling in the carbachol-induced activation of the proteases trypsin an

175 e via Epac1 but is also involved in CCK- and carbachol-induced amylase release, with their action mos

176 nd that compound 6 is effective in reversing carbachol-induced contraction in the isolated strip prep

177 When rise of [Ca(2+)]pm was prevented, the carbachol-induced DAG and PKC responses were somewhat re

178 um responses in cortical neurons and affects carbachol-induced depletion of PIP2.

179 These carbachol-induced effects were associated with increased

180 In mice with recurrent seizures, carbachol-induced enhancement of spontaneous IPSCs (sIPS

181 reduction of PTEN expression did not affect carbachol-induced externalization of TRPC6 but increased

182 Specifically, we show that carbachol-induced gamma oscillations (25-35 Hz) in rat h

183 ically identified CA1 and CA3 neurons during carbachol-induced gamma oscillations in mouse hippocampa

184 al potential measurements suggested that the carbachol-induced inward current was mediated mainly by

185 location of TRPC6 to the plasma membrane and carbachol-induced net Ca(2+) entry into T6.11 cells.

186 We found that carbachol-induced oscillations in rat CA3 have biphasic

187 0Hz range, and for the kainate-, but not the carbachol-induced oscillations, there was a small but si

188 re we compare the properties of kainate- and carbachol-induced oscillatory activity generated in CA3

189 Imatinib inhibited the carbachol-induced PCs of both juvenile and adult denuded

190 In contrast to WT, bradykinin- or carbachol-induced reduction in MVO2 was attenuated in nN

191 HHcy significantly decreased bradykinin- or carbachol-induced reduction of myocardial oxygen consump

192 Thus, carbachol-induced reversal of sevoflurane anesthesia rep

193 ted salivary gland inflammation and enhanced carbachol-induced saliva secretion.

194 by PIK-93, LY294002, or wortmannin decreased carbachol-induced translocation of TRPC6 to the plasma m

195 Carbachol-induced vasodilatation was increased in arteri

196 cting endothelin-induced vasoconstriction or carbachol-induced vasorelaxation.

197 Effects of carbachol infusion on patterns of neuronal activation du

198 Consistent with this idea, the ACh agonist carbachol inhibited presynaptic specialization of motorn

199 The carbachol-initiated phosphorylation of Ser(23) alpha1 su

200 found that dialyzing the cholinergic agonist carbachol into HVC increased the pitch, amplitude, tempo

201 xample, injection of the cholinergic agonist carbachol into the dorsomedial pons produces an REM slee

202 t direct infusion of the cholinergic agonist carbachol into the striatum, but not into the neighborin

203 ld refraction was measured before and during carbachol iontophoresis stimulated accommodation, a tota

204 his reaction are of special interest because carbachol is an isosteric analogue of the physiological

205 2 induced by the muscarinic receptor agonist carbachol is mediated by a signaling axis comprising pho

206 We found that carbachol is more effective at increasing REM sleep when

207 nd the arrestins also significantly enhanced carbachol-mediated activation of extracellular signal-re

208 in a significant decrease in thapsigargin or carbachol-mediated Ca(2+) influx.

209 GRK6, but not GRK5, significantly increased carbachol-mediated calcium mobilization.

210 2 or arrestin-3 also significantly increased carbachol-mediated calcium mobilization.

211 mM, but was decreased by 40 mM glucose, and carbachol-mediated dilation was unaffected.

212 Also, carbachol-mediated inhibition of NHE3 activity was aboli

213 showed that gadolinium-, thapsigargin-, and carbachol-mediated release of Ca(2+)(i) induced Shh expr

214 that modest doses of the cholinergic agonist carbachol normally decorrelate spontaneous activity gene

215 nsity) and endothelium-dependent dilatation (carbachol) of the MCA were not different between groups.

216 icantly augmented the stimulatory effects of carbachol on H508 cell proliferation and p90RSK activati

217 rts and significantly enhanced the effect of carbachol on inhibition of spontaneous action potential

218 aic acid eliminated the inhibitory effect of carbachol on isoproterenol-stimulated NCX current, indic

219 e the effects of baroreflex, chemoreflex and carbachol on pacemaker entrainment and electrical conduc

220 nd recorded pre- and postsynaptic effects of carbachol on SLDsp neurons.

221 ctin activity strongly reduced the effect of carbachol on the elongation of all the neurites, whereas

222 ied the general cholinergic receptor agonist carbachol onto neurons in dorsolateral PFC (DLPFC) of ma

223 eptor or epidermal growth factor receptor by carbachol or epidermal growth factor stimulation induced

224 on currents activated by bath application of carbachol or intracellular infusion of GTPgammaS, demons

225 reduce GDNF secretion, while treatment with carbachol or long-term electrical stimulation enhances G

226 5' triphosphate (BzATP), cholinergic agonist carbachol, or the activator of conventional and novel PK

227 a1 was not blocked by PKC inhibitors, unlike carbachol- or phorbol 12-myristate 13-acetate-initiated

228 logical "two-concentration" acetylcholine or carbachol paradigm was developed and validated to determ

229 With increasing times during carbachol perfusion of glands, in situ, PKC-alpha redist

230 ield stimulation, as well as activation with carbachol, phenylephrine, and KCl, were lower in old tha

231 Interactions among carbachol, PKC inhibitors, phorbol 12-myristate 13-aceta

232 l stimulation, indicating that the siRNA and carbachol portions of the conjugate retained their funct

233 Consistent with this, carbachol potentiated GIP-mediated insulin release from

234 In contrast, carbachol produced a prolonged period of reduced capacit

235 ive parotid cells isoproterenol enhanced the carbachol-promoted increases in [Ca(2+)](i) and oxygen c

236 e inhibitor ouabain reduced and enhanced the carbachol-promoted phosphorylation of Ser(23) and Ser(16

237 vation of ADAM10 with the muscarinic agonist carbachol promotes PrP(C) shedding and reduces the bindi

238 nduced sensitization of cholecystokinin- and carbachol-regulated Ca(2+) signaling in pancreatic acina

239 generated less force in response to KCl and carbachol relative to the levels in control murine BSM s

240 relaxed rapidly with comparable rates after carbachol removal and only 1.5-fold slower after KCl rem

241 orthosteric binding pocket caused a loss of carbachol response that could be rescued by BQCA.

242 nsient activation of muscarinic receptors by carbachol results in a long-lasting depression of synapt

243 Stimulation of M3R with carbachol significantly increased this association.

244 Carbachol stimulated the formation of disulfide bonds in

245 , stimulated with forskolin, stimulated with carbachol, stimulated with substance P, and, as a test f

246 This was associated with a reduction in carbachol-stimulated amylase release and an accumulation

247 also abrogates the ability of EGF to inhibit carbachol-stimulated basolateral K(+) currents.

248 re, we show that, in addition to suppressing carbachol-stimulated Ca(2+) release, Gbeta5-RGS7 enhance

249 g effects of ethanol on cholecystokinin- and carbachol-stimulated Ca(2+) signaling and intracellular

250 In the presence of this peptide, carbachol-stimulated calcium inhibition of NHE3 was lost

251 Carbachol-stimulated Cl(-) efflux and the protein levels

252 f extracellular Ca(2+), also reduced TG- and carbachol-stimulated ERK1/2 phosphorylation.

253 In contrast to mucus release, PGE(2)- and carbachol-stimulated fluid secretion was not dependent o

254 ist SCH-23390 (100 microM) did not alter the carbachol-stimulated glutamate release even though it in

255 ulline (10 microM) into the SN prolonged the carbachol-stimulated glutamate release in similar fashio

256 Carbachol-stimulated glutamate release was prolonged by

257 The P2X7 antagonist did not alter the carbachol-stimulated increase in [Ca2+]i or peroxidase.

258 n intestinal CaCC based on inhibition of ATP/carbachol-stimulated iodide influx in HT-29 cells after

259 eated cells, the inhibitory effect of EGF on carbachol-stimulated K(+) channel activity was lost.

260 Inhibition of PKC partially inhibited carbachol-stimulated MAPK activation while completely in

261 Chelation of Ca(2+) also partially inhibited carbachol-stimulated MAPK with no effect on phenylephrin

262 Prostaglandin E(2) (PGE(2))- and carbachol-stimulated mucus release was severely inhibite

263 e release by 60% and reduced CCK- as well as carbachol-stimulated pancreatic amylase release by 40%.

264 The c-src inhibitor PP1 inhibited carbachol-stimulated phosphorylation of Pyk2.

265 M(inh)-23 strongly inhibited spontaneous and carbachol-stimulated rhythmic contractions.

266 Inhibition of classical PKC proteins blocked carbachol-stimulated Ser(23) alpha1 subunit phosphorylat

267 Carbachol stimulation releases Gbetagamma subunits from

268 evation of intracellular calcium levels upon carbachol stimulation seen in these cells.

269 ide injection, the antinociceptive effect of carbachol stimulation was blocked.

270 of endocytosis at levels similar to those of carbachol stimulation, indicating that the siRNA and car

271 ity, irrespective of whether it is evoked by carbachol, store depletion, lanthanides or elevated intr

272 e opening rate for a subsaturating dosage of carbachol, suggesting that physostigmine does not intera

273 stinal peptide and/or forskolin but not with carbachol; synergy was absent in CF glands.

274 PCLS from Rgs5(-/-) mice contracted more to carbachol than those from WT mice, indicating that RGS5

275 r deactivation was significantly faster with carbachol than with acetylcholine and was significantly

276 imulation with concentrations of glucose and carbachol that accelerate hydrolysis of endogenous AA fr

277 ore stimulation with the cholinergic agonist carbachol, the alpha(1D)-adrenergic agonist phenylephrin

278 In bronchi precontracted by carbachol, the IP receptor agonist cicaprost induced pro

279 -protein-coupled muscarinic receptor mimetic carbachol, the phorbol ester phorbol 12-myristate 13-ace

280 itions but after elevation of [Ca(2+)](i) by carbachol, this overlap was abolished.

281 hat they may contact different residues than carbachol to activate M(1) but occupy substantially over

282 The ability of pontine carbachol to elicit any cortical, hippocampal or brainst

283 Finally, by applying carbachol to increase EPSC activity, we observed that cl

284 further corroborated by the inefficiency of carbachol to increase IPSC frequency in these cells.

285 dB SPL, 4h) before and after application of carbachol to the DCN surface.

286 These constants for the binding of carbachol to the P-site are about an order of magnitude

287 Specifically, Ca(2+) entry seen after carbachol treatment in cells transiently expressing TRPC

288 rce generation during the first 2 mins after carbachol treatment), and myosin light chain phosphoryla

289 ifferences in sustained responses to KCl and carbachol treatments and washouts, respectively.

290 moderate differences in response to KCl and carbachol treatments, and relaxed rapidly with comparabl

291 The excitatory effect of carbachol was blocked by antagonists of M1 and M3 muscar

292 sphosphate production by cholecystokinin and carbachol was inefficient in Mist1-/- cells.

293 The cholinergic agonist carbachol was infused into the medial septum, and hippoc

294 Carbachol was synthesized with an active choline group a

295 l NO synthase in response to the M3R agonist carbachol were diminished.

296 pressure elevation and IKACh sensitivity to carbachol were enhanced in Ex16 rats, implicating both c

297 ves in the presence of low concentrations of carbachol, which probably increased the tonic level of I

298 the synergistic combination of forskolin and carbachol, which produced near-maximal clearance rates r

299 initiated by the muscarinic receptor agonist carbachol, which promoted an increase to approximately 5

300 ependent FRET response for acetylcholine and carbachol with M(3)-AChR-N514Y.