The Action of Acetylcholine on the Rabbit Auricle*

Webb, John

doi:10.1111/j.1476-5381.1950.tb00584.x

Cited by 29 publications

(12 citation statements)

References 49 publications

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“…When this concentration was applied in the presence of eserine 10-6 g./ml., the contractions were arrested. This effect of eserine was described by Webb (1950). The contractions were resumed when the bath fluid was changed.…”

Section: Resultsmentioning

confidence: 85%

Quinidine and Anticholinesterases on Rabbit Auricles

Briscoe¹,

Burn²

1954

British Journal of Pharmacology and Chemotherapy

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In a recent paper Burn and Kottegoda (1953) have described the action of eserine on the isolated auricles of the rabbit heart. They found that in most preparations low concentrations decreased the rate of beating, though in some they increased the rate. Higher concentrations always decreased the rate and finally arrested the contractions, and then the auricles were found to be electrically inexcitable. The effect on the amplitude of contraction was different, for low and medium concentrations increased it; high concentrations, however, reduced it. It was stated that the effect of eserine was likely to be that of an anticholinesterase, since DFP had a similar action on the rate leading to arrest of the beat, while neostigmine in high concentration had a different action, increasing the rate, neostigmine being known (e.g., from the work of Riker and Wescoe, 1946) to have an action of its own in addition to its action as an anticholinesterase.In the following account we describe some experiments which appear to relate the action of high concentrations of eserine to the action of quinidine, and we describe also the effect of various other anticholinesterases on the auricles. We have also examined the effect of (1946) that it is a substance which has been shown to reduce the action of acetylcholine (ACh) in all forms of muscle. Thus in the presence of quinidine not only the stimulant action of ACh on the frog rectus and the rabbit intestine is reduced, but also the inhibitory action on the rabbit auricles.A small concentration of ACh (0.16 x 1O-" g./ml.) caused a slight inhibition of rabbit auricles as shown in Fig. 1. When this concentration was applied in the presence of eserine 10-6 g./ml., the contractions were arrested. This effect of eserine was described by Webb (1950). The contractions were resumed when the bath fluid was changed. The arrest was produced a second time by the same concentrations of eserine and ACh, and quinidine (1.5 x 10-g./ml.) was then added. The contractions began again. This result was contractions of isolated auricles in 35 ml. bath. At A 0 6 fsg. ACh. At W the d was changed. At E, eserine 10-6 g./ml. At Q, 0-5 mg. quinidine was added. The numbers above the record are the rate per min.

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Section: Resultsmentioning

confidence: 85%

Quinidine and Anticholinesterases on Rabbit Auricles

Briscoe¹,

Burn²

1954

British Journal of Pharmacology and Chemotherapy

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“…The selectivity observed with acetylcholine is probably attributable to the action ofAChE, since such selectivity was abolished in the presence of physostigmine. Webb (1950) found high concentrations of AChE in mycardial nodal tissue. The 40-60 fold difference in affinity of a bridged analogue of arecoline reported by Mutschler & Lambrecht (1984) may also be attributable to the action of AChE.…”

Section: Discussionmentioning

confidence: 90%

Action of agonists and antagonists at muscarinic receptors present on ileum and atria in vitro

Clague

Eglen

Strachan

et al. 1985

British J Pharmacology

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1 The action of 'selective' agonists and antagonists at muscarinic receptors mediating ileal contractions, and the rate and force of atrial contractions has been assessed. 2 The effect of nicotinic receptor stimulation, catecholamine release and acetylcholinesterase (AChE) action on muscarinic activity has also been assessed. 3 The nicotinic actions of carbachol did not affect its agonist potency nor the antagonist affinity data obtained when this agonist was used in atrial and ileal preparations. 4 Antagonist data indicated that muscarinic receptors mediating the rate and force of atrial contractions did not differ. Differences in agonist potencies at these two muscarinic receptors were attributable to either differences in intrinsic efficacy or susceptibility to the action of acetylcholinesterase. The small differences in agonist potency observed between atrial and ileal muscarinic receptors were considered not sufficient to indicate receptor heterogeneity. 5 The pirenzepine affinity data indicated that all three receptors are of the M2 type. Affinity data using secoverine and 4-diphenyl-acetoxy-N-methyl piperidine methiodide indicated that ileal and atrial muscarinic receptors differ. Data obtained using gallamine, pancuronium and stercuronium cannot be regarded as indicative of receptor affinity since the antagonism is not competitive; it did nonetheless corroborate the conclusion that ileal and atrial muscarinic receptors are different.

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“…Although, except for carbachol, there was reasonable agreement with respect to order of potency, all the compounds were more potent relative to acetylcholine in depressing ventricular rate than atrial force. The difference may reflect the type and/or distribution of cardiac cholinesterase enzymes which control the quantitative response of the myocardium to acetylcholine (Webb, 1950). If, as is suggested, there is a greater concentration of cholinesterase activity in the region of the pacemaker than in contractile muscle cells (Webb, 1950;Roberts & Konjovic, 1969), then not only would a larger concentration of acetylcholine be needed to inhibit rate than force, but also differences in relative potencies would be expected between acetylcholine and those compounds not hydrolyzed by cholinesterases.…”

Section: Drugs Usedmentioning

confidence: 99%

Effects of several muscarinic agonists on cardiac performance and the release of noradrenaline from sympathetic nerves of the perfused rabbit heart

Fozard

Muscholl²

1972

British J Pharmacology

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Summary1. The effects of several muscarinic agonists on atrial tension development, ventricular rate and noradrenaline release from terminal sympathetic fibres evoked by electrical nerve stimulation (SNS) and 1,1-dimethyl-4-phenylpiperazinium (DMPP) were measured in isolated perfused rabbit hearts. 2. Hexamethonium, in a concentration which almost abolished the release of noradrenaline by DMPP, had no effect on the release produced by SNS, confirming that the stimulation was postganglionic.3. The order of potency for inhibition of atrial tension development was N-methyl-1,2,5,6, tetrahydro-nicotinic acid prop-2-yne ester (MH-l)>oxo-tremorine > acetylcholine > methacholine > carbachol> furtrethonium> pilocarpine>4-(m-chlorophenylcarbamoyloxy)-2-butynyltrimethylammoniumchloride (McN-A-343)>N-benzyl-3-pyrrolidyl acetate methobromide (AHR 602). All effects were abolished by atropine (1-4 x 10-6M). 4. Each compound was more potent relative to acetylcholine in inhibiting ventricular rate than atrial tension. With the exception of carbachol, the order of potency was the same. 5. Both AHR 602 and McN-A-343 facilitated the release of noradrenaline by SNS and inhibited that by DMPP. The effects were atropine-resistant and hence non-muscarinic. 6. The muscarinic compounds (except AHR 602 and McN-A-343) each produce atropine-sensitive inhibition of noradrenaline release evoked both by SNS and DMPP although it is likely that furtrethonium and pilocarpine have additional non-muscarinic inhibitory activity against DMPP. The order of potency on both parameters and the potencies relative to acetylcholine were in good agreement with those for inhibition of atrial tension. 7. The results suggest that similar muscarinic receptors mediate inhibition of atrial tension development, ventricular rate and neuronal noradrenaline release caused by SNS and DMPP.8. In terms of the two muscarinic sites known to be present in the superior cervical ganglion, the receptors of the terminal fibres mediating inhibition of noradrenaline release are more likely to correspond to those mediating hyperpolarization than to those mediating depolarization, for which AHR 602 and McN-A-343 show specificity.

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The Action of Acetylcholine on the Rabbit Auricle*

Cited by 29 publications

References 49 publications

Quinidine and Anticholinesterases on Rabbit Auricles

Quinidine and Anticholinesterases on Rabbit Auricles

Action of agonists and antagonists at muscarinic receptors present on ileum and atria in vitro

Effects of several muscarinic agonists on cardiac performance and the release of noradrenaline from sympathetic nerves of the perfused rabbit heart

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