Receptor mediated presynaptic modulation of the release of noradrenaline in human papillary muscle

Ida Matkó, E. Fehér, E. Vízi

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Objective: The aim was to determine the presynaptic modulation of noradrenaline (NA) release from the sympathetic nerve terminals in human isolated papillary muscle. Methods: Papillary muscle and the right atrial appendage were obtained from operations on 22 patients (10 men and 12 women). The papillary muscle preparations were preincubated with [3H]NA and the release of [3H] at rest and in response to field stimulation was measured. Results: Using an immunohistochemical method dopamine-β-hydroxylase-positive neurones were found in the papillary muscle and right atrial appendage sample. The release of noradrenaline from the papillary muscle, associated with axonal activity, was enhanced by 7,8(methylenedioxy)-14-α-hydroxyalloberbane HC1 (CH-38083). a selective α2 adrenoceptor antagonist, and inhibited by xylazine, an α2 adrenoceptor agonist, indicating that negative feedback modulation was functioning. In addition, the release of [3H]NA was enhanced by atropine, pancuronium, and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), a selective M3muscarinic receptor antagonist, and reduced by oxotremorine, a selective muscarinic receptor agonist, indicating that acetylcholine released from the parasympathetic nerve ending was able to reach the varicose noradrenergic axon terminals that are equipped with inhibitory M3 muscarinic receptors. Conclusions: These findings, obtained for the first time in human papillary muscle, indicate that the release of noradrenaline is modulated by α2 autoreceptors activated by noradrenaline and M, muscarinic heteroreceptors. Thus during parasympathetic stimulation the release of noradrenaline from the sympathetic axon terminals is presynaptically controlled through muscarinic receptors.Cardiovascular Research 1994;28:700-704.

Original languageEnglish
Pages (from-to)700-704
Number of pages5
JournalCardiovascular Research
Volume28
Issue number5
DOIs
Publication statusPublished - Jan 1 1994

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Presynaptic Receptors
Papillary Muscles
Norepinephrine
Atrial Appendage
Presynaptic Terminals
Muscarinic Receptors
Adrenergic Receptors
Muscarinic M3 Receptors
Oxotremorine
Xylazine
Pancuronium
Muscarinic Agonists
Autoreceptors
Nerve Endings
Mixed Function Oxygenases
Atropine
Cholinergic Agents
Acetylcholine
Dopamine
Neurons

Keywords

  • Human papillary muscle
  • Muscarinic M3 heteroreceptors
  • Pancuronium
  • Presynaptic modulation
  • [3H]noradrenaline release
  • α2 autoreceptors

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

Receptor mediated presynaptic modulation of the release of noradrenaline in human papillary muscle. / Matkó, Ida; Fehér, E.; Vízi, E.

In: Cardiovascular Research, Vol. 28, No. 5, 01.01.1994, p. 700-704.

Research output: Contribution to journalArticle

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abstract = "Objective: The aim was to determine the presynaptic modulation of noradrenaline (NA) release from the sympathetic nerve terminals in human isolated papillary muscle. Methods: Papillary muscle and the right atrial appendage were obtained from operations on 22 patients (10 men and 12 women). The papillary muscle preparations were preincubated with [3H]NA and the release of [3H] at rest and in response to field stimulation was measured. Results: Using an immunohistochemical method dopamine-β-hydroxylase-positive neurones were found in the papillary muscle and right atrial appendage sample. The release of noradrenaline from the papillary muscle, associated with axonal activity, was enhanced by 7,8(methylenedioxy)-14-α-hydroxyalloberbane HC1 (CH-38083). a selective α2 adrenoceptor antagonist, and inhibited by xylazine, an α2 adrenoceptor agonist, indicating that negative feedback modulation was functioning. In addition, the release of [3H]NA was enhanced by atropine, pancuronium, and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), a selective M3muscarinic receptor antagonist, and reduced by oxotremorine, a selective muscarinic receptor agonist, indicating that acetylcholine released from the parasympathetic nerve ending was able to reach the varicose noradrenergic axon terminals that are equipped with inhibitory M3 muscarinic receptors. Conclusions: These findings, obtained for the first time in human papillary muscle, indicate that the release of noradrenaline is modulated by α2 autoreceptors activated by noradrenaline and M, muscarinic heteroreceptors. Thus during parasympathetic stimulation the release of noradrenaline from the sympathetic axon terminals is presynaptically controlled through muscarinic receptors.Cardiovascular Research 1994;28:700-704.",
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N2 - Objective: The aim was to determine the presynaptic modulation of noradrenaline (NA) release from the sympathetic nerve terminals in human isolated papillary muscle. Methods: Papillary muscle and the right atrial appendage were obtained from operations on 22 patients (10 men and 12 women). The papillary muscle preparations were preincubated with [3H]NA and the release of [3H] at rest and in response to field stimulation was measured. Results: Using an immunohistochemical method dopamine-β-hydroxylase-positive neurones were found in the papillary muscle and right atrial appendage sample. The release of noradrenaline from the papillary muscle, associated with axonal activity, was enhanced by 7,8(methylenedioxy)-14-α-hydroxyalloberbane HC1 (CH-38083). a selective α2 adrenoceptor antagonist, and inhibited by xylazine, an α2 adrenoceptor agonist, indicating that negative feedback modulation was functioning. In addition, the release of [3H]NA was enhanced by atropine, pancuronium, and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), a selective M3muscarinic receptor antagonist, and reduced by oxotremorine, a selective muscarinic receptor agonist, indicating that acetylcholine released from the parasympathetic nerve ending was able to reach the varicose noradrenergic axon terminals that are equipped with inhibitory M3 muscarinic receptors. Conclusions: These findings, obtained for the first time in human papillary muscle, indicate that the release of noradrenaline is modulated by α2 autoreceptors activated by noradrenaline and M, muscarinic heteroreceptors. Thus during parasympathetic stimulation the release of noradrenaline from the sympathetic axon terminals is presynaptically controlled through muscarinic receptors.Cardiovascular Research 1994;28:700-704.

AB - Objective: The aim was to determine the presynaptic modulation of noradrenaline (NA) release from the sympathetic nerve terminals in human isolated papillary muscle. Methods: Papillary muscle and the right atrial appendage were obtained from operations on 22 patients (10 men and 12 women). The papillary muscle preparations were preincubated with [3H]NA and the release of [3H] at rest and in response to field stimulation was measured. Results: Using an immunohistochemical method dopamine-β-hydroxylase-positive neurones were found in the papillary muscle and right atrial appendage sample. The release of noradrenaline from the papillary muscle, associated with axonal activity, was enhanced by 7,8(methylenedioxy)-14-α-hydroxyalloberbane HC1 (CH-38083). a selective α2 adrenoceptor antagonist, and inhibited by xylazine, an α2 adrenoceptor agonist, indicating that negative feedback modulation was functioning. In addition, the release of [3H]NA was enhanced by atropine, pancuronium, and 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP), a selective M3muscarinic receptor antagonist, and reduced by oxotremorine, a selective muscarinic receptor agonist, indicating that acetylcholine released from the parasympathetic nerve ending was able to reach the varicose noradrenergic axon terminals that are equipped with inhibitory M3 muscarinic receptors. Conclusions: These findings, obtained for the first time in human papillary muscle, indicate that the release of noradrenaline is modulated by α2 autoreceptors activated by noradrenaline and M, muscarinic heteroreceptors. Thus during parasympathetic stimulation the release of noradrenaline from the sympathetic axon terminals is presynaptically controlled through muscarinic receptors.Cardiovascular Research 1994;28:700-704.

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