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

Abstract

[3H]‐noradrenaline ([3H]‐NA) release from the main pulmonary artery of the rabbit has been measured in the presence of neuronal (cocaine, 3 × 10−5 M) and extraneuronal (corticosterone, 5 × 10−5 M) uptake blockers. Removal of K from the external medium increased the [3H]‐NA release. In the absence of external K, ouabain (10−4 M) 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. 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. 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. 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 (30 min). In both cases the initial delay of ouabain action was greatly shortened. 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.

[3H]noradrenaline release from rabbit pulmonary artery: sodium‐pump‐dependent sodium‐calcium exchange.

“…After a delay (90-120 min), however, the [3H]NA release started to increase again (see , which seems to be the result of Ca2+ release from internal stores caused by [Na+]i, probably by a Na-Ca exchange mechanism (Baker & Crawford, 1975;Carafoli & Crompton, 1978;Baker & Di Polo, 1984;T6r6k et al 1984;T6r6k & Magyar, 1986). In the sympathetic nerves of the pulmonary artery, the internal ions cannot be measured.…”

“…At the end of the washing period the flow rate was changed to 4 ml min-' and the extraneuronal-uptake blocker corticosterone (5 x 10-5 M) was also added to the Krebs solution. Endo, Starke, Bangerter & Taube (1977) (Torok et al 1984;Magyar et al 1986; Fig. 1 added.…”

“…The method has been described previously (Borowski, Starke, Ehrl & Endo, 1977;Torok et al 1984;Torok & Magyar, 1986;Magyar et al 1986 [3H]NA: 4-2-4-6 x 10-7M) for 45 min (pargyline and the NA-stabilizing agents ascorbic acid, 3 x 10-4 M, and disodium EDTA, 3 x 10-5 M) were present. The temperature of the Krebs solution was 37 'C.…”

“…The method has been described previously (Borowski, Starke, Ehrl & Endo, 1977;Torok et al 1984;Torok & Magyar, 1986;Magyar et al 1986). Briefly, after the preparation had been placed in Krebs solution, 25 psl [3H]NA was added to the incubation solution (final concentration of TABLE 1.…”

Tissue noradrenaline and the polyol pathway in experimentally diabetic rats

“…Acute inhibition of Na', K+-ATPase has been found to increase both acetylcholine and NA turnover (Vizi et al, 1982;Magyar et al, 1986).…”