Effect of atropine and acetylcholine on nerve stimulated output of noradrenaline and dopamine-beta-hydroxylase from isolated rabbit and guinea pig hearts

Langley, Albert E.; Gardier, Robert W.

doi:10.1007/bf00509269

Cited by 13 publications

(5 citation statements)

References 18 publications

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“…Vagal release of ACh can reduce noradrenaline release in the atrium (18), resulting in inhibition of sympathetic output (16, 19, 20, 22, 23, 25). To determine the origin of the FTR @60 , we have used ␤-adrenergic antagonists to block sympathetic input.…”

Section: Discussionmentioning

confidence: 99%

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Mann

Hoyt

Feldman

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Central regulation of cardiac output via the sympathetic and parasympathetic branches of the autonomic nervous system allows the organism to respond to environmental changes. Sudden onset stimuli, startle stimuli, are useful probes to study central regulatory responses to the environment. In mammals, startle stimuli induce a transient bradycardia that habituates with repeated stimulation. Repeated presentation of the stimulus results in tachycardia. In this study, we investigate the behavioral regulation of heart rate in response to sudden stimuli in the zebrafish. Larval zebrafish show a stereotyped heart rate response to mild electrical shock. Naïve fish show a significant increase in interbeat interval that resolves in the 2 s following stimulation. This transient bradycardia decreases on repeated exposure to the stimulus. Following repeated stimulation, the fish become tachycardic within 1 min of stimulation. Both the transient bradycardia and following tachycardia responses are blocked with administration of the ganglionic blocker hexamethonium, demonstrating that these responses are mediated centrally. The transient bradycardia is blocked by the muscarinic antagonist atropine, suggesting that this response is mediated by the parasympathetic system, while the following tachycardia is specifically blocked by the beta-adrenergic antagonist propranolol, suggesting that this response is mediated by the sympathetic nervous system. Together, these results demonstrate that at the larval stage, zebrafish actively regulate cardiac output to changes in their environment using both the parasympathetic and sympathetic branches of the autonomic nervous system, a behavioral response that is markedly similar to that observed in mammals to similar sudden onset stimuli. cardiac regulation; zebrafish AUTONOMIC DYSREGULATION APPEARS to play a key role in the development of cardiovascular disease (14), and genetic factors are hypothesized to contribute to the variable progression of the disease (30, 34). The startle response can be used as a probe for autonomic regulation of cardiac activity (4, 7). Both parasympathetic and sympathetic responses to the startle stimulus can be observed, which allows for both components of the autonomic nervous system to be probed with a single behavioral manipulation. This study seeks to establish the zebrafish larvae as a model organism to investigate autonomic regulation of cardiac activity by developing a rapid behavioral assay to probe for autonomic regulation and dysregulation of the cardiac output.In mammals, sudden onset stimuli induce a rapid change in behavior that consists of both locomotor activity and coincident autonomic behavioral changes. The locomotor activity, the startle response, may be characterized by a complex motor response involving contraction of the muscles of the eyelid, neck, and limbs [reviewed in (15)]. In rats, for example, an air-puff stimulus results in a stereotyped motor response and transient bradycardia (7). Repeated exposure to the stimulus results in decre...

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Section: Discussionmentioning

confidence: 99%

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Mann

Hoyt

Feldman

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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“…It is known that both exogenous acetylcholine and vagal stimulation are able to reduce the amount of noradrenaline released on cardiac sympathetic nerve stimulation, in isolated atrial preparations (Langley & Gardier, 1977;Muscholl, 1980) and in anaesthetized dogs (Levy & Blattberg, 1975;Lavallee, de Champlain, Nadeau & Yamaguchi, 1978; Levy, 1984). In dogs, stimulation of the right cardioaccelerator nerves caused an increase in coronary sinus noradrenaline levels.…”

Section: Introductionmentioning

confidence: 99%

Sympathetic‐parasympathetic interactions at the heart, possibly involving neuropeptide Y, in anaesthetized dogs.

Revington

McCloskey

1990

The Journal of Physiology

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SUMMARY1. Stimulation of cardiac sympathetic nerves caused prolonged inhibition of vagal effects on heart rate, an effect which has been proposed on the basis of previous studies to be due to neuropeptide Y or a neuropeptide Y-like substance, released from the sympathetic nerves.2. This prolonged vagal inhibitory effect was attenuated or abolished when the sympathetic stimulation responsible was given together with continuous vagal stimulation.3. Continuous vagal stimulation alone did not modify the ability of administered neuropeptide Y to cause inhibition of cardiac vagal action.4. The results are consistent with the cardiac vagal nerves releasing a transmitter (probably acetylcholine) which acts on cardiac sympathetic nerve endings, inhibiting them from releasing neuropeptide Y or a neuropeptide Y-like substance.

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“…The present paper was aimed at resolving an apparent discrepancy: why should acetylcholine fail to inhibit the evoked [3H]-noradrenaline overflow from guineapig atria (Story et al, 1975), when, in contrast, acetylcholine inhibits the evoked noradrenaline (Lindmar et al, 1968) or [3H]-noradrenaline overflow (Westfall & Hunter, 1974;Langley & Gardier, 1977) from guinea-pig perfused hearts? We adopted similar, though not identical methodology to that described by McCulloch et al (1974) which was used in the paper reporting the lack of muscarinic inhibition by acetylcholine (Story et al, 1975 (Illes et al, 1984).…”

Section: Discussionmentioning

confidence: 97%

“…Results obtained with the whole perfused guinea-pig heart in which a presynaptic muscarinic inhibition was observed (Westfall & Hunter, 1974;Langley & Gardier, 1977) rendered the lack of muscarinic receptors in atria an unlikely cause for the lack of inhibition by acetylcholine. Thus, the reason for the apparent discrepancy between findings with acetylcholine in atria vs. whole heart remained obscure.…”

Section: Introductionmentioning

confidence: 96%

“…One (among others) possible explanation for carinic receptors appears to be a general rule as such finding could be a lack of presynaptic muscarinic noradrenaline release from virtually all peripheral receptors and such a model would then represent an tissues investigated could be inhibited by muscarinic interesting tool potentially useful in the investigation i) The Macmillan Press Ltd 1985 of muscarinic mechanisms. Results obtained with the whole perfused guinea-pig heart in which a presynaptic muscarinic inhibition was observed (Westfall & Hunter, 1974;Langley & Gardier, 1977) rendered the lack of muscarinic receptors in atria an unlikely cause for the lack of inhibition by acetylcholine. Thus, the reason for the apparent discrepancy between findings with acetylcholine in atria vs. whole heart remained obscure.…”

Section: Introductionmentioning

confidence: 96%

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Cholinesterase activity and exposure time to acetylcholine as factors influencing the muscarinic inhibition of [³H]‐noradrenaline overflow from guinea‐ pig isolated atria

Fuder

Muscholl

Wolf

1985

British J Pharmacology

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1 Guinea-pig isolated atria were incubated and loaded with [3H]-noradrenaline. The release of 3H and of [3H]-noradrenaline was induced by field stimulation (6-9 trains of 150 pulses at 5 Hz). The stimulation-evoked overflows of 3H and of [3H]-noradrenaline were determined. 2 In the absence of an inhibitor of acetylcholinesterase, acetylcholine (12 min preincubation before nerve stimulation, up to 10pM) failed to inhibit the evoked [3H]-noradrenaline overflow. In the presence of atropine, an increase by acetylcholine of evoked release was observed in the same atria. In contrast, the selective muscarinic agonist methacholine significantly decreased the evoked overflow. 6 It is concluded that a muscarinic inhibition by acetylcholine (upon prolonged exposure time) may be masked by a concomitant facilitation of release and/or desensitization of the muscarinic inhibitory mechanism. Furthermore, degradation by acetylcholinesterase contributes in part to the ineffectiveness of acetylcholine as a presynaptic inhibitor. When a distortion of the overflow/release ratio was excluded, adrenergic and nicotinic effects were prevented, and acetylcholinesterase was inhibited, the fading of muscarinic inhibition by acetylcholine may have been exclusively due to a slow and moderate desensitization of the presynaptic muscarinic mechanism.

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Effect of atropine and acetylcholine on nerve stimulated output of noradrenaline and dopamine-beta-hydroxylase from isolated rabbit and guinea pig hearts

Cited by 13 publications

References 18 publications

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Sympathetic‐parasympathetic interactions at the heart, possibly involving neuropeptide Y, in anaesthetized dogs.

Cholinesterase activity and exposure time to acetylcholine as factors influencing the muscarinic inhibition of [³H]‐noradrenaline overflow from guinea‐ pig isolated atria

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Effect of atropine and acetylcholine on nerve stimulated output of noradrenaline and dopamine-beta-hydroxylase from isolated rabbit and guinea pig hearts

Cited by 13 publications

References 18 publications

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Cardiac response to startle stimuli in larval zebrafish: sympathetic and parasympathetic components

Sympathetic‐parasympathetic interactions at the heart, possibly involving neuropeptide Y, in anaesthetized dogs.

Cholinesterase activity and exposure time to acetylcholine as factors influencing the muscarinic inhibition of [3H]‐noradrenaline overflow from guinea‐ pig isolated atria

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Cholinesterase activity and exposure time to acetylcholine as factors influencing the muscarinic inhibition of [³H]‐noradrenaline overflow from guinea‐ pig isolated atria