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H Majewski

Publications and source records attributed to H Majewski.

At least 73 records · Page 4Linked to original sources
PubMed1981

An interaction between prejunctional alpha-adrenoceptors and prejunctional beta-adrenoceptors.

The ability os isoprenaline to enhance transmitter release from sympathetic nerves in rat atria incubated with [3H]noradrenaline was assessed under three conditions of prejunctional alpha-adrenoceptor activation: in the presence of phentolamine, in the presence of noradrenaline, and in the absence of either drug. Isoprenaline-induced enhancement of transmitter release was inversely related to the degree of activation of prejunctional alpha-adrenoceptors. Thus there appears to be an interaction between the prejunctional alpha-adrenoceptor inhibitory mechanism and the prejunctional beta-adrenoceptor facilitatory mechanism. In rabbit ear arteries incubated with [3H]noradrenaline, isoprenaline facilitated transmitter release in the presence but not in the absence of phentolamine. Therefore in some tissues it may be necessary to block prejunctional alpha-adrenoceptors before prejunctional beta-adrenoceptors can be demonstrated.

Animals↗
PubMed1981

Adrenaline-induced hypertension in rats.

1. Rats implanted with osmotic minipumps delivering adrenaline intraperitoneally at the rate of 2.9 nmol/h had significantly higher systolic and diastolic pressures from days 2 to 6 after implantation than sham-operated controls rats. 2. Concomitant treatment with metoprolol tartrate (2.5 mg/kg, intraperitoneally, twice daily) prevented the elevation in blood pressure induced by adrenaline from osmotic minipumps. Such metoprolol treatment did not affect the blood pressure of controls rats. 3. Noradrenaline administered intraperitoneally from osmotic minipumps at the rate of 2.9 nmol/h had no significant effect on blood pressure over a 6-day period of observation. 4. Tachyphylaxis developed to the acute pressor responses to intermittent intravenous infusions of adrenaline in doses of 0.78 microgram (4.24 nmol) every 10 min, but after 14 days of such treatment systolic and diastolic blood pressures were significantly greater than in controls rats. 5. It is suggested that the increase in blood pressure produced by chronic treatment with adrenaline is due to the uptake and accumulation of adrenaline in noradrenergic nerve terminals, from which it is subsequently released as a cotransmitter that mediates a positive feedback loop on transmission by acting on prejunctional beta-adrenoceptors.

Animals↗
PubMed1981

Activation of prejunctional beta-adrenoceptors in rat atria by adrenaline applied exogenously or released as a co-transmitter.

1 Adrenaline (10 nM) significantly enhanced the stimulation-induced efflux of radioactivity from rat atria previously incubated with [3H]-noradrenaline ([3H]-NA). This effect was abolished by metoprolol (.01 muM). 2 Adrenaline in a higher concentration (1 muM) and NA (1 muM) significantly reduced the stimulation-induced efflux of radioactivity. However, in the presence of phenoxybenzamine (10 muM), adrenaline (1 muM) enhanced the efflux, whereas NA (1 muM) had no effect. 3 In rat isolated atria pre-incubated with adrenaline and then incubated with NA, both catecholamines were taken up and were released by field stimulation. When pre-incubation was with adrenaline and incubation was with [3H]-NA, metoprolol decreased the stimulation-induced efflux of radioactivity. This effect did not occur if the atria were pre-incubated with NA instead of adrenaline, suggesting tht neuronally released adrenaline activates prejunctional beta-adrenoceptors. 4 In conscious rats, intravenously administered adrenaline (6.0 and 0.6 nmol/kg) was taken up and retained in the atria and could be released by field stimulation. The release was calcium-dependent from these rats up to 24 h after administration.

Animals↗
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↗