Metabolic Requirements for the Uptake of Noradrenaline by Isolated Atria and Vas Deferens of the Rabbit

Paton, David M.

doi:10.1159/000136275

Cited by 19 publications

(5 citation statements)

References 14 publications

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“…In the present study, metabolic inhibition was produced by omission of D-glucose from the medium and by exposure of tissues to 100% nitrogen and 10 mm sodium azide. Previous studies (Paton, 1972a) have shown that the net uptake of noradrenaline by adrenergic nerves in rabbit atria is only markedly reduced by simultaneous inhibition of both glycolysis and oxidation via the Krebs cycle. Metabolic inhibition so produced was found to produce a rapid, very marked increase in efflux that was maxinmal All tissues were exposed to 100% N2, 10-2M sodium azide and omission of D-glucose from 60-100 minutes.…”

Section: S(c) Cocaine and Desipraminementioning

confidence: 90%

“…The loss of tissue K+ so produced was not modified by the addition of lidocaine, cocaine or desipramine. (f) Metabolic inhibition the net uptake of noradrenaline by rabbit atria was abolished by metabolic inhibition, possibly as a result of inhibition of coupled Na+-K+ pumping (Paton, 1972a). According to the Na+-gradient hypothesis, metabolic inhibition should act primarily by increasing efflux (Schultz & Curran, 1970).…”

Section: (D) Temperaturementioning

confidence: 99%

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Mechanism of efflux of noradrenaline from adrenergic nerves in rabbit atria

Paton

1973

British J Pharmacology

164

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Summary1. The mechanism of efflux of (-)-[3H]-noradrenaline was examined in rabbit atria, which were pretreated with reserpine and pargyline. 2. Between 40 and 100 min, efflux occurred predominantly from a single intraneuronal compartment.3. Efflux was rapidy increased by (-)-and (+)-noradrenaline, tyramine and (±)-metaraminol, but not by (±)-isopropylnoradrenaline or (±)-normetanephrine. The increase in efflux produced by (-)-noradrenaline was inhibited by cocaine and desipramine but not by lidocaine. 4. Spontaneous effluxes, and those accelerated by (-)-noradrenaline, were temperature-sensitive. 5. Effiux was increased by ouabain, omission of K+, metabolic inhibition and lowering of the external Na± concentration. These effects were significantly reduced by cocaine and desipramine but not by lidocaine. 6. These findings provide evidence that the effiux of [3H]-noradrenaline from adrenergic nerves occurs by a cocaine-sensitive, carrier-mediated process. The characteristics of the efflux process are compatible with, but not conclusive proof for, the Na+-gradient hypothesis.

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Section: S(c) Cocaine and Desipraminementioning

confidence: 90%

Section: (D) Temperaturementioning

confidence: 99%

Mechanism of efflux of noradrenaline from adrenergic nerves in rabbit atria

Paton

1973

British J Pharmacology

164

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“…Perfusion with lactate as substrate led to a greater release of NA than with glucose. This may possibly be explained by a better energy preservation within the neuron when glucose is used as substrate (Paton 1972, Wakade & Furchgott, 1968.…”

Section: Discussionmentioning

confidence: 99%

Ischaemia‐induced release of noradrenaline and creatine kinase in the isolated, working rat heart

Carlsson

Abrahamsson²,

Almgren³

et al. 1987

Acta Physiologica Scandinavica

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In order to examine an early ischaemia-induced local release of myocardial noradrenaline (NA), the left coronary artery of the isolated working rat heart was ligated for periods varying between 7.5 min and 30 min, followed by reperfusion for 5 min. As perfusion substrate, glucose, lactate or both were used. In part of the experiments, hearts were pre-labelled with [3H]NA. Already after 7.5 min of ischaemia, an increased efflux of endogenous NA was observed in the perfusate at reperfusion, concomitant with a decrease in tissue NA content. This effect was most pronounced with lactate as substrate. Qualitatively similar effects were seen on [3H]NA efflux from labelled hearts. The combination of glucose and lactate as substrate markedly reduced (compared with lactate alone) the efflux of NA, whereas no such reduction was observed on the efflux of creatine kinase (CK). It is concluded that ischaemia is associated with an early local release of NA. Furthermore, ischaemia may induce different effects on the metabolic processes of the myocyte as compared with the adrenergic nerve ending.

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“…To inhibit the mono amine oxidase, pargyline (10 flM) was added to the medium throughout the experiments. All hearts were first perfused with normal medium for 10 min and then perfused for 20 min with one of the following media con taining tyramine (10 SaM): normal medium (control), normoxic buffer containing 10 mM sucrose instead of glucose (glucose deprivation), the medium aerated with a mixture of 95% N2 and 5% CO2 (anoxia), anoxic medium containing 10 mM sucrose instead of glucose (anoixa with glucose deprivation) (7). In the preliminary experi ments, the NA overlfow at 10 ,uM of tyramine was higher than that at 5 ,eM and was similar to that at 50 ,uM.…”

mentioning

confidence: 99%