Unterschiede zwischen Tyramin und Dimethylphenylpiperazin in der Ca++-Abhängigkeit und im zeitlichen Verlauf der Noradrenalin-Freisetzung am isolierten Kaninchenherzen

Lindmar, R.; Löffelholz, K.; Muscholl, E.

doi:10.1007/bf02136230

Cited by 68 publications

(12 citation statements)

References 10 publications

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“…These results confirm previous reports that sympathetic transmitter release evoked by DMPP is calcium-dependent (Lindmar et al, 1967;Haeusler et al, 1969;Chubb et al, 1972;Thoa et al, 1975). The demonstration that release by 5-HT is, like DMPP, dependent on extracellular calcium ion has its counterpart in the perfused cat adrenal gland, where catecholamine release evoked both by nicotinic agonists and 5-HT was abolished by omission of calcium from the perfusion medium (Douglas & Rubin, 1963;Poisner & Douglas, 1966).…”

Section: Discussionsupporting

confidence: 93%

“…In the case of nicotinic agonists colchicine has been specifically suggested to interfere with some step(s) in an excitation-secretion coupling mechanism which is calcium ion-dependent and which results in the release of noradrenaline, probably by exocytosis from the noradrenergic nerve terminals (Smith & Winkler, 1972;Sorimachi et al, 1973). The present results suggest a similar conclusion would be justified with 5-HT as the stimulus to release, especially as responses to tyramine, whose action is independent of both extracellular calcium ion and the process of exocytosis (Lindmar et al, 1967;Thoenen, Huerlimann & Haefely, 1969;Chubb, De Potter & De Schaepdryver, 1972;Thoa, Wooten, Axelrod & Kopin, 1975) remained largely unaffected by perfusion with colchicine ( Figure 3).…”

Section: Discussionsupporting

confidence: 64%

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Mechanism of the Indirect Sympathomimetic Effect of 5‐hydroxytryptamine on the Isolated Heart of the Rabbit

Fozard

Mwaluko

1976

British J Pharmacology

142

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1 Rabbit isolated hearts, perfused by the Langendorff technique, were used to investigate the indirect sympathomimetic effects of 5-hydroxytryptamine (5-HT). Comparisons were made with noradrenaline and with two indirectly acting sympathomimetic agents with entirely different mechanisms of action, tyramine and dimethylphenylpiperazinium (DMPP). 2 The cardiac stimulant effects of 5-HT, tyramine and DMPP were inhibited by propranolol and practolol and the pA2 values obtained were similar to those obtained with noradrenaline as the agonist. 3 Responses to 5-HT, tyramine and DMPP were greatly reduced on hearts from rabbits pretreated with 6-hydroxydopamine. Such hearts had less than 7% of their normal catecholamine concentration and no fluorescence characteristic of noradrenaline in the cardiac sympathetic nerves could be demonstrated. 4 Rapid, reversible and selective tachyphylaxis to 5-HT was demonstrated during perfusion with 5-HT. In hearts desensitized to DMPP by perfusion with DMPP, responses to 5-HT were also reduced. S Perfusion of hearts with colchicine inhibited stimulant responses to 5-HT and DMPP but had little effect on responses to noradrenaline or tyramine. 6 Desmethylimipramine enhanced cardiac stimulant responses to noradrenaline and to a lesser extent, those to 5-HT and DMPP. Responses to tyramine were consistently inhibited by desmethylimipramine. 7 Tetrodotoxin abolished responses of the heart to electrical nerve stimulation but left responses to noradrenaline, 5-HT and DMPP unaffected. 8 5-HT, tyramine and DMPP evoked 3H-release from hearts whose neuronal noradrenaline stores had been labelled by perfusion with [3HI-(-)-noradrenaline. The pattern of release evoked by 5-HT was similar to that of DMPP but differed from that of tyramine.9 Reducing the calcium concentration in the Tyrode solution from 3.6 to 0.2 mEq/l did not affect 3H-overflow after tyramine but greatly inhibited that evoked by 5-HT and DMPP.10 The results confirm that the stimulant effects of 5-HT on the rabbit isolated heart are the result of noradrenaline release. They further suggest that the site of the release is the terminal sympathetic nerve network. The mechanism of release shows more similarities to that of DMPP (calcium-dependent depolarization and exocytosis) than to that of tyramine (neuronal uptake and stoichiometric displacement).

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 64%

Mechanism of the Indirect Sympathomimetic Effect of 5‐hydroxytryptamine on the Isolated Heart of the Rabbit

Fozard

Mwaluko

1976

British J Pharmacology

142

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“…Tyramine Release of NA by tyramine is also a calcium-independent process; presumably it acts by displacing NA from storage sites in sympathetic nerves (Lindmar, Loffelholz & Muscholl, 1967). Table 1 shows that guanidine did not affect [3H]-NA release induced by tyramine (0.1 mM).…”

Section: Perfusion and Incubation Solutionsmentioning

confidence: 94%

Effect of Guanidine on Release of Noradrenaline From the Perfused Spleen of the Cat

Hirsch¹,

Kirpekar²,

Prat³

1979

British J Pharmacology

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1 Guanidine increased noradrenaline (NA) output at 5 Hz by 3 to 6 fold, and doubled it at 30 Hz. Onset of maximum activity was slow, and reversal was also slow. Output of NA induced by potassium, sodium deprivation, or tyramine was not affected. 2 NA output was doubled at low concentrations (1 to 2 mM) of guanidine, but maximal effect was obtained at 4 mM. At 10 mM, spontaneous release was occasionally observed. 3 The effect of guanidine on NA release was related to the external calcium concentration. Outputs which previously have been shown to be insignificant at 5 Hz in 0.25 and 0.75 mm calcium-Krebs solution were markedly enhanced by guanidine. Guanidine enhanced release at all calcium concentrations up to 7.5 mm, but maximum output was obtained at 2.5 mm. 4 Guanidine had no effect on the recovery of intra-arterially infused NA. 5 The effects of guanidine and tetraethyl-ammonium (TEA) on NA release at 5 Hz were additive. 6 Guanidine reversed the inhibition of NA release by guanethidine during nerve stimulation at 5 and 10 Hz, and the NA output increased nearly 2.5 fold after repeated stimulation of the nerves. Guanidine was less effective in reversing the inhibitory effects of guanethidine on NA release at 30 Hz. 7 Guanidine did not affect release of catecholamines (CA) from the perfused cat adrenal gland by splanchnic nerve stimulation. 8 It is suggested that guanidine enhances NA release partly by increasing the influx of calcium into the neurone during an action potential, and also by interfering with intracellular binding ot calcium.

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“…In contrast, the tyramine-induced release of noradrenaline is unaffected by a-adrenoceptor agonists or antagonists (Starke & Montel, 1974). Tyramine and nerve stimulationinduced noradrenaline release differ in that tyramineinduced release is not calcium-dependent (Lindmar, Loffelholz & Muscholl, 1967). Accordingly, it has been suggested that stimulation of the presynaptic a-adrenoceptors somehow reduces the accumulation of intraneuronal free calcium and thus prevents the electrosecretory coupling process (Stjarne, 1973;Starke & Montel, 1974).…”

mentioning

confidence: 99%

The EFFECT OF DIFFERENT CALCIUM CONCENTRATIONS ON THE INHIBITORY EFFECT OF PRESYNAPTIC Α‐ADRENOCEPTORS IN THE RAT VAS DEFERENS

Drew

1978

British J Pharmacology

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Unterschiede zwischen Tyramin und Dimethylphenylpiperazin in der Ca++-Abhängigkeit und im zeitlichen Verlauf der Noradrenalin-Freisetzung am isolierten Kaninchenherzen

Cited by 68 publications

References 10 publications

Mechanism of the Indirect Sympathomimetic Effect of 5‐hydroxytryptamine on the Isolated Heart of the Rabbit

Mechanism of the Indirect Sympathomimetic Effect of 5‐hydroxytryptamine on the Isolated Heart of the Rabbit

Effect of Guanidine on Release of Noradrenaline From the Perfused Spleen of the Cat

The EFFECT OF DIFFERENT CALCIUM CONCENTRATIONS ON THE INHIBITORY EFFECT OF PRESYNAPTIC Α‐ADRENOCEPTORS IN THE RAT VAS DEFERENS

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