The Mechanism of Action of Indirectly Acting Sympathomimetic Amines

Trendelenburg, U.; Langeloh, Augusto; Bönisch, Heinz

doi:10.1007/978-3-642-46625-0_5

Cited by 50 publications

(19 citation statements)

References 35 publications

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“…Although tyramine induced a marked efflux of axoplasmic NA, it caused an increase in dialysate DHPG levels which subsequently returned to control levels. As the neuronal NA uptake mechanism is inhibited during the administration of tyramine ( Bönisch & Trendelenburg 1988), our result suggest that the net effect of NA leakage and tyramine‐induced mobilization compensate for the alteration of axoplasmic NA evoked by carrier‐mediated outward NA transport, while, in the pretreatment with reserpine, the efflux of NA evoked by tyramine was associated with a reduction of DHPG. When reserpine inhibited vesicle transport of NA and reduced NA graduation between the axoplasma and the vesicle, outward efflux of NA (evoked by tyramine) is greater than NA leakage and mobilization from stored NA vesicle.…”

Section: Discussionmentioning

confidence: 76%

“…Therefore, the source of the increment in dialysate NA is considered to be derived from the regional neuroeffector junction, adjacent myocardial cell and surrounding vasculature. Tyramine might be accumulated by the neuronal and extraneuronal spaces ( Bönisch & Trendelenburg 1988, Marino et al . 1992 ).…”

Section: Discussionmentioning

confidence: 99%

“…To compare the tyramine‐induced NA response between an in vitro and in vivo state, we had to examine the effect of the pretreatment with reserpine and pargyline on the dialysate NA response to tyramine, because most in vitro experiments were performed after inhibition of vesicle NA uptake and MAO ( Bönisch & Trendelenburg 1988, Parker & Cubeddu 1988). In the previous studies, we examined the efflux of NA after pretreatment with reserpine and pargyline ( Yamazaki et al .…”

Section: Discussionmentioning

confidence: 99%

“…1987 ). The mechanism of action of sympathomimetic amine has been well documented ( Bönisch & Trendelenburg 1988). A pronounced release of NA from a nerve ending is achieved when a substrate of uptake 1 induces a brisk outward transport of NA, which is maintained by an ability of the substrate to mobilize vesicularly stored NA.…”

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confidence: 99%

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Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Takauchi

Yamazaki

Akiyama

2000

Acta Physiologica Scandinavica

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With the use of dialysis technique, the effects of tyramine on in situ cardiac sympathetic nerve endings were examined in anaesthetized cats. Dialysis probes were implanted in the left ventricular myocardium, and the concentration of dialysate noradrenaline (NA) served as an indicator of NA output at the cardiac sympathetic nerve ending. Locally applied tyramine (600 microM) increased dialysate NA levels from 17 +/- 1 (pg mL-1) to 3466 +/- 209 (pg mL-1). Pretreatment with reserpine (vesicle transport NA blocker 1 microM) did not affect tyramine-induced NA efflux. The tyramine-induced NA efflux was augmented by pretreatment with pargyline (1 mM) but suppressed by pargyline (10 mM). Pretreatment with alpha-methyl-tyrosine suppressed NA efflux evoked by tyramine. These pretreatments did not affect the time course of NA efflux but only altered peak height of NA efflux. The efflux of NA evoked by tyramine was not associated with any reduction of dihydroxyphenylglycol (DHPG). In contrast, in the pretreatment with reserpine, the efflux of NA was associated with a reduction of DHPG. This result suggests that NA graduation between axoplasm and stored vesicle contributes to maintaining the axoplasmic NA level during carrier-mediated outward NA transport. The tyramine-induced NA efflux provides a close reflection of the NA content at the nerve ending. With the use of dialysis, this experimental model is suitable for studying the mechanism of sympathomimetic amine-induced neurotransmitter efflux.

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Section: Discussionmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Takauchi

Yamazaki

Akiyama

2000

Acta Physiologica Scandinavica

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“…The first group includes transportable PEAs, which are close to NE in both structure and physicochemical properties. These PEAs serve as substrates for MTs [1,2], and their transport via a neuronal membrane is mediated by the formation of substrate -MT complexes. The second group includes nontransportable PEAs.…”

Section: Introductionmentioning

confidence: 99%

Comparative Molecular Model Estimation of the Affinity of Phenylethylamines to the Binding Sites of Membrane Transporters

Al'tshuler

2005

Pharm Chem J

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Factors determining the difference in the affinity of phenylethylamines (PEAs) to the binding sites of membrane transporters have been studied using the molecular models of PEA enantiomers built in preferred conformations for such binding. In the molecules of PEA enantiomers having planar anti conformations, the substituents at asymmetric (chiral) atoms interacting with the binding sites can occur in different, favorable or unfavorable, configuration-dependent positions. By estimating the positions of such substituents in a biophase, it is possible to explain the relationship between the structure and the affinity.

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Examination of the action of 3,4-methylenedioxymethamphetamine on rat A10 dopamine neurons

Gifford

Minabe

Toor

et al. 1996

Synapse

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Extracellular single cell recording was used to examine the effect of intravenous administration of (−), (+), and (±)‐3,4‐methylenedioxymethamphetamine (MDMA) on A10 dopamine (DA) neurons in chloral hydrate anesthetized male rats. Both (±)‐MDMA and (+)‐MDMA inhibited the firing rate of most (79%) A10 DA cells. By contrast, (−)‐MDMA induced either no effect or a slight increase in the firing rate of these cells. Analysis of the effects of (±)‐MDMA on the firing pattern of the DA cells revealed an overall decrease in the percentage of spikes in bursts but both increases and decreases were seen in the coefficient of variation of interspike intervals. To determine the contribution of 5‐HT and DA to the (±)‐MDMA‐induced inhibition of A10 DA cells rats were pretreated either with the 5‐HT synthesis inhibitor p‐chlorophenylalanine (PCPA) or the DA synthesis inhibitor α‐methyl‐p‐tyrosine (AMPT). Pretreatment of rats with PCPA did not reduce the ability of (±)‐MDMA to inhibit the DA cells. However, in rats pretreated with AMPT, the (±)‐MDMA‐induced inhibition was blocked and some cells (44%) showed instead an increase in firing rate following administration of (±)‐MDMA. The administration of l‐3,4‐dihydroxyphenylalanine (L‐DOPA) to AMPT‐treated rats rapidly restored the inhibition of cell firing by (±)‐MDMA. In conclusion, the results reported here demonstrate that MDMA has an overall inhibitory effect on A10 DA cells. Despite MDMA's greater potency in releasing 5‐HT compared to DA, the inhibitory effect of this drug on A10 DA cells appears to be mediated by the latter transmitter. © 1996 Wiley‐Liss, Inc.

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The Mechanism of Action of Indirectly Acting Sympathomimetic Amines

Cited by 50 publications

References 35 publications

Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Tyramine‐induced endogenous noradrenaline efflux from in situ cardiac sympathetic nerve ending in cats

Comparative Molecular Model Estimation of the Affinity of Phenylethylamines to the Binding Sites of Membrane Transporters

Examination of the action of 3,4-methylenedioxymethamphetamine on rat A10 dopamine neurons

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