The action of excess potassium and calcium on ouabain-evoked [3H]-noradrenaline release from the rabbit pulmonary artery

K. Magyar, T. T. Nguyen, T. L. Torok, P. T. Toth

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

1. [3H]-noradrenaline ([3H]-NA) release from the main pulmonary artery of the rabbit has been measured in the presence of neuronal (cocaine, 3 x 10-5M) and extraneuronal (corticosterone, 5 x 10-5M) uptake blockers. 2. Removal of K from the external medium increased the [3H]-NA release. In the absence of external K, ouabain (10-4M) further enhanced the neurotransmitter release. The 'K-free' stimulated [3H]-NA release was inhibited by an increase of external Ca (7.5 mM), an action antagonized by ouabain. 3. After preperfusion of the preparations for 30 min with either excess K (23.6 mM) or excess Ca (7.5 mM), the ouabain-stimulated [3H]-NA release was inhibited by about 50%; the rates of inhibition did not differ significantly from each other. However, the characteristic initial delay before ouabain-evoked neurotransmitter release was shortened in excess K, and prolonged in excess Ca-containing solution. 4. When both excess K and Ca were applied together 30 min before ouabain perfusion, the action of ouabain in releasing neurotransmitter was also inhibited but the rate of inhibition did not differ significantly from that seen when K or Ca were applied separately. The action of K in shortening the initial delay was partly antagonized by Ca. 5. Excess Ca antagonized the inhibition of ouabain-stimulated [3H]-NA release caused by excess K when Ca and ouabain were applied together after 30 min preperfusion with excess K-containing solution. Again excess Ca failed to inhibit the ouabain-evoked neurotransmitter release if ouabain and excess K were applied together after excess Ca preperfusion (3 min). In both cases the initial delay of the ouabain action was greatly shortened. 6. The results suggest a Na-Ca competition at the external activation site of the nerve terminal sodium-pump similar to that of Na-K competition. Furthermore it seems that there is a sort of K-Ca competition as well, suggested by the finding that excess Ca prevented the inhibition caused by excess K of ouabain-evoked noradrenaline release and vice versa.

Original languageEnglish
Pages (from-to)63-71
Number of pages9
JournalBritish Journal of Pharmacology
Volume87
Issue number1
Publication statusPublished - 1986

Fingerprint

Ouabain
Pulmonary Artery
Norepinephrine
Potassium
Rabbits
Calcium
Neurotransmitter Agents
Sodium-Potassium-Exchanging ATPase
Corticosterone
Cocaine
Perfusion

ASJC Scopus subject areas

  • Pharmacology

Cite this

The action of excess potassium and calcium on ouabain-evoked [3H]-noradrenaline release from the rabbit pulmonary artery. / Magyar, K.; Nguyen, T. T.; Torok, T. L.; Toth, P. T.

In: British Journal of Pharmacology, Vol. 87, No. 1, 1986, p. 63-71.

Research output: Contribution to journalArticle

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abstract = "1. [3H]-noradrenaline ([3H]-NA) release from the main pulmonary artery of the rabbit has been measured in the presence of neuronal (cocaine, 3 x 10-5M) and extraneuronal (corticosterone, 5 x 10-5M) uptake blockers. 2. Removal of K from the external medium increased the [3H]-NA release. In the absence of external K, ouabain (10-4M) further enhanced the neurotransmitter release. The 'K-free' stimulated [3H]-NA release was inhibited by an increase of external Ca (7.5 mM), an action antagonized by ouabain. 3. After preperfusion of the preparations for 30 min with either excess K (23.6 mM) or excess Ca (7.5 mM), the ouabain-stimulated [3H]-NA release was inhibited by about 50{\%}; the rates of inhibition did not differ significantly from each other. However, the characteristic initial delay before ouabain-evoked neurotransmitter release was shortened in excess K, and prolonged in excess Ca-containing solution. 4. When both excess K and Ca were applied together 30 min before ouabain perfusion, the action of ouabain in releasing neurotransmitter was also inhibited but the rate of inhibition did not differ significantly from that seen when K or Ca were applied separately. The action of K in shortening the initial delay was partly antagonized by Ca. 5. Excess Ca antagonized the inhibition of ouabain-stimulated [3H]-NA release caused by excess K when Ca and ouabain were applied together after 30 min preperfusion with excess K-containing solution. Again excess Ca failed to inhibit the ouabain-evoked neurotransmitter release if ouabain and excess K were applied together after excess Ca preperfusion (3 min). In both cases the initial delay of the ouabain action was greatly shortened. 6. The results suggest a Na-Ca competition at the external activation site of the nerve terminal sodium-pump similar to that of Na-K competition. Furthermore it seems that there is a sort of K-Ca competition as well, suggested by the finding that excess Ca prevented the inhibition caused by excess K of ouabain-evoked noradrenaline release and vice versa.",
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N2 - 1. [3H]-noradrenaline ([3H]-NA) release from the main pulmonary artery of the rabbit has been measured in the presence of neuronal (cocaine, 3 x 10-5M) and extraneuronal (corticosterone, 5 x 10-5M) uptake blockers. 2. Removal of K from the external medium increased the [3H]-NA release. In the absence of external K, ouabain (10-4M) further enhanced the neurotransmitter release. The 'K-free' stimulated [3H]-NA release was inhibited by an increase of external Ca (7.5 mM), an action antagonized by ouabain. 3. After preperfusion of the preparations for 30 min with either excess K (23.6 mM) or excess Ca (7.5 mM), the ouabain-stimulated [3H]-NA release was inhibited by about 50%; the rates of inhibition did not differ significantly from each other. However, the characteristic initial delay before ouabain-evoked neurotransmitter release was shortened in excess K, and prolonged in excess Ca-containing solution. 4. When both excess K and Ca were applied together 30 min before ouabain perfusion, the action of ouabain in releasing neurotransmitter was also inhibited but the rate of inhibition did not differ significantly from that seen when K or Ca were applied separately. The action of K in shortening the initial delay was partly antagonized by Ca. 5. Excess Ca antagonized the inhibition of ouabain-stimulated [3H]-NA release caused by excess K when Ca and ouabain were applied together after 30 min preperfusion with excess K-containing solution. Again excess Ca failed to inhibit the ouabain-evoked neurotransmitter release if ouabain and excess K were applied together after excess Ca preperfusion (3 min). In both cases the initial delay of the ouabain action was greatly shortened. 6. The results suggest a Na-Ca competition at the external activation site of the nerve terminal sodium-pump similar to that of Na-K competition. Furthermore it seems that there is a sort of K-Ca competition as well, suggested by the finding that excess Ca prevented the inhibition caused by excess K of ouabain-evoked noradrenaline release and vice versa.

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