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Biomedical subjects

H Majewski

Publications and source records attributed to H Majewski.

At least 91 records · Page 5Linked to original sources
PubMed1980

Adrenaline activation of prejunctional beta-adrenoceptors in guinea-pig atria.

1. Adrenaline in a concentration of 1.0 microM depressed the stimulation-induced efflux of tritium from the guinea-pig atria incubated with [3H]-noradrenaline, whereas adrenaline in a concentration of 0.5 nM significantly enhanced the stimulation-induced efflux of tritium. This enhancement was blocked by metoprolol (0.1 microM) and thus appears to be mediated by beta-adrenoceptors. 2. In guinea-pig atria incubated with unlabelled adrenaline and then with [3H]-noradrenaline, both catecholamines were released by field stimulation. In such atria metoprolol, practolol, oxprenolol or propranolol decreased the stimulation-induced efflux of tritium. These effects did not occur if the atria were incubated with unlabelled noradrenaline and then with [3H]-noradrenaline, suggesting that neuronally released adrenaline activates prejunctional beta-adrenoceptors. 3. The effect of oxprenolol in decreasing the release of tritium from guinea-pig atria, incubated with unlabelled adrenaline and then with [3H]-noradrenaline was greater in the presence of phentolamine. This may reflect the alpha-adrenoceptor blocking activity of oxprenolol.

Animals↗
PubMed1980

Mechanism of noradrenaline release from rabbit atria induced by nicotinic agonists.

The release of noradrenaline and its metabolic products by the nicotinic agonists nicotine, 1,1-dimethyl-4-phenylpiperazinium (DMPP) and acetylcholine (in the presence of atropine) was investigated in rabbit atria in which the transmitter stores were labelled with (3H)-noradrenaline. The proportions of noradrenaline and its metabolic products released by nicotine (50 microM), DMPP (100 microM) and acetylcholine (1.6 mM, in the presence of atropine (6 microM)) were similar to those released by sympathetic nerve stimulation: (3H)-noradrenaline itself comprised more than 90% of the tritiated compounds released by these agents. None of the nicotinic agonists affected the activity of monoamine oxidase extracted from rabbit atria. The results suggest that nicotinic agonists and sympathetic nerve stimulation release noradrenaline from the same sites and by similar mechanisms, presumably by exocytosis of the contents of transmitter storage vesicles.

Acetylcholine↗
PubMed1979

Modulation of sympathetic transmission by neuronally-released dopamine.

1 When rabbits were pretreated with Fla-63, there was a marked inhibition of dopamine-beta-hydroxylase such that, after incubation of the ear arteries with [3H]-dopamine 47.2% of the tritium in the tissue was retained as unchanged dopamine. 2 [3H]-dopamine was released by stimulation of the sympathetic nerves in ear arteries taken from rabbits pretreated with Fla-63 and incubated with [3H]-dopamine. 3 The dopamine antagonists metoclopramide (1.0 microM) and ergometrine (1.0 microM) enhanced the stimulation-induced efflux of tritium in ear arteries taken from rabbits pretreated with Fla-63 and incubated with [3H]-dopamine, but not when the arteries were incubated with [3H]-noradrenaline. 4. These results suggest that if dopamine is present in the transmitter stores, it can be released by stimulation of the sympathetic nerves, and if the amount is adequate, it can activate an inhibitory feedback loop where prejunctional dopamine receptors are present.

Animals↗