Opiate agonists inhibit noradrenaline release via opiate B-receptors and N-cyclopropylmethylnorazidomorphine (CAM). Blocks electrically evoked contractions via histamine in the mouse vas deferens

J. Knoll, L. Kerecsen, G. T. Somogyi, A. Kovacs

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Abstract

N-cyclopropylmethylnorazidomorphine (CAM) reduced slightly the stimulation evoked 3H-noradrenaline outflow from the mouse vas deferens and this effect was not antagonized by naloxone. Azidomorphine, however, inhibited potently the release of noradrenaline and the effect was completely antagonized by CAM and naloxone. The field stimulation induced release of acetylcholine remained unchanged in the presence of CAM. Atropine leaving the release of noradrenaline unchanged caused 50-60% inhibition of responses to electrical stimulation. Histamine and 48/80 inhibited the twitch responses to electrical stimulation and this effect was antagonized by H1-receptor antagonists (mepyramine, chloropyramine, phenindamine, thenalidine, cyprohepatdine), but not by cimetidine. H1-receptor antagonists increased the release of noradrenaline and facilitated neuromuscular transmission; cimetidine was ineffective. H1-blocking antihistamines completely inhibited the blockade of the electrically evoked contractions caused by CAM, whereas cimetidine left them unaltered. The effects of morphine and azidomorphine were only moderately antagonized by H1-blocking antihistamines and the effect of methionine enkephalin remained unchanged. In the presence of atropine and H1-blocking antihistamines CAM antagonized the effect of the opiate agonists competitively. It was concluded that in the mouse vas deferens opiate agonists inhibit noradrenaline release via opiate B-receptors. CAM inhibits the twitch responses in this test via histamine and H1-receptors were found to be involved in this mechanism.

Original languageEnglish
Pages (from-to)52-65
Number of pages14
JournalArchives Internationales de Pharmacodynamie et de Therapie
Volume251
Issue number1
Publication statusPublished - 1981

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Opiate Alkaloids
Vas Deferens
Opioid Receptors
Histamine
Norepinephrine
Histamine H1 Receptors
Histamine Antagonists
Cimetidine
Naloxone
Atropine
Electric Stimulation
Pyrilamine
Methionine Enkephalin
Morphine
Acetylcholine
N-cyclopropylmethylnorazidomorphine

ASJC Scopus subject areas

  • Pharmacology

Cite this

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title = "Opiate agonists inhibit noradrenaline release via opiate B-receptors and N-cyclopropylmethylnorazidomorphine (CAM). Blocks electrically evoked contractions via histamine in the mouse vas deferens",
abstract = "N-cyclopropylmethylnorazidomorphine (CAM) reduced slightly the stimulation evoked 3H-noradrenaline outflow from the mouse vas deferens and this effect was not antagonized by naloxone. Azidomorphine, however, inhibited potently the release of noradrenaline and the effect was completely antagonized by CAM and naloxone. The field stimulation induced release of acetylcholine remained unchanged in the presence of CAM. Atropine leaving the release of noradrenaline unchanged caused 50-60{\%} inhibition of responses to electrical stimulation. Histamine and 48/80 inhibited the twitch responses to electrical stimulation and this effect was antagonized by H1-receptor antagonists (mepyramine, chloropyramine, phenindamine, thenalidine, cyprohepatdine), but not by cimetidine. H1-receptor antagonists increased the release of noradrenaline and facilitated neuromuscular transmission; cimetidine was ineffective. H1-blocking antihistamines completely inhibited the blockade of the electrically evoked contractions caused by CAM, whereas cimetidine left them unaltered. The effects of morphine and azidomorphine were only moderately antagonized by H1-blocking antihistamines and the effect of methionine enkephalin remained unchanged. In the presence of atropine and H1-blocking antihistamines CAM antagonized the effect of the opiate agonists competitively. It was concluded that in the mouse vas deferens opiate agonists inhibit noradrenaline release via opiate B-receptors. CAM inhibits the twitch responses in this test via histamine and H1-receptors were found to be involved in this mechanism.",
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T1 - Opiate agonists inhibit noradrenaline release via opiate B-receptors and N-cyclopropylmethylnorazidomorphine (CAM). Blocks electrically evoked contractions via histamine in the mouse vas deferens

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AU - Kerecsen, L.

AU - Somogyi, G. T.

AU - Kovacs, A.

PY - 1981

Y1 - 1981

N2 - N-cyclopropylmethylnorazidomorphine (CAM) reduced slightly the stimulation evoked 3H-noradrenaline outflow from the mouse vas deferens and this effect was not antagonized by naloxone. Azidomorphine, however, inhibited potently the release of noradrenaline and the effect was completely antagonized by CAM and naloxone. The field stimulation induced release of acetylcholine remained unchanged in the presence of CAM. Atropine leaving the release of noradrenaline unchanged caused 50-60% inhibition of responses to electrical stimulation. Histamine and 48/80 inhibited the twitch responses to electrical stimulation and this effect was antagonized by H1-receptor antagonists (mepyramine, chloropyramine, phenindamine, thenalidine, cyprohepatdine), but not by cimetidine. H1-receptor antagonists increased the release of noradrenaline and facilitated neuromuscular transmission; cimetidine was ineffective. H1-blocking antihistamines completely inhibited the blockade of the electrically evoked contractions caused by CAM, whereas cimetidine left them unaltered. The effects of morphine and azidomorphine were only moderately antagonized by H1-blocking antihistamines and the effect of methionine enkephalin remained unchanged. In the presence of atropine and H1-blocking antihistamines CAM antagonized the effect of the opiate agonists competitively. It was concluded that in the mouse vas deferens opiate agonists inhibit noradrenaline release via opiate B-receptors. CAM inhibits the twitch responses in this test via histamine and H1-receptors were found to be involved in this mechanism.

AB - N-cyclopropylmethylnorazidomorphine (CAM) reduced slightly the stimulation evoked 3H-noradrenaline outflow from the mouse vas deferens and this effect was not antagonized by naloxone. Azidomorphine, however, inhibited potently the release of noradrenaline and the effect was completely antagonized by CAM and naloxone. The field stimulation induced release of acetylcholine remained unchanged in the presence of CAM. Atropine leaving the release of noradrenaline unchanged caused 50-60% inhibition of responses to electrical stimulation. Histamine and 48/80 inhibited the twitch responses to electrical stimulation and this effect was antagonized by H1-receptor antagonists (mepyramine, chloropyramine, phenindamine, thenalidine, cyprohepatdine), but not by cimetidine. H1-receptor antagonists increased the release of noradrenaline and facilitated neuromuscular transmission; cimetidine was ineffective. H1-blocking antihistamines completely inhibited the blockade of the electrically evoked contractions caused by CAM, whereas cimetidine left them unaltered. The effects of morphine and azidomorphine were only moderately antagonized by H1-blocking antihistamines and the effect of methionine enkephalin remained unchanged. In the presence of atropine and H1-blocking antihistamines CAM antagonized the effect of the opiate agonists competitively. It was concluded that in the mouse vas deferens opiate agonists inhibit noradrenaline release via opiate B-receptors. CAM inhibits the twitch responses in this test via histamine and H1-receptors were found to be involved in this mechanism.

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