The key role of sodium in the ouabain-mediated potentiation of potassium-evoked catecholamine release in cat adrenal glands.

1. The effect of [Na]o on the catecholamine release evoked by K in ouabain pretreated, isolated adrenal glands of the cat, was investigated. 2. Reduction of [Na]o to 70, 50 and 25 mM, with sucrose as a substitute, did not modify the spontaneous catecholamine release but progressively increased the K (17.7 mM)-evoked secretory response. 3. Ouabain pretreatment (100 microM; 10 min) greatly increased the K (17.7 mM)-evoked catecholamine secretory response in glands perfused with normal Krebs. Such an increase was still seen in glands perfused with 70 mM Na-containing solution but disappeared when [Na]o was reduced to 25 and 10 mM. 4. Preperfusion of non-ouabain treated glands with Li-enriched Krebs, for a 40 min period, caused an increase in the K (17.7 mM)-evoked secretory response which was dependent on [Li]o and essentially similar to that induced by ouabain pretreatment. 5. Ouabain treatment (100 microM; 10 min) of glands perfused with normal Krebs evoked a long lasting catecholamine release, which reached a plateau at about 36 min and amounted to 0.68 +/- 0.25 microgram 2 min-1 (n = 9). Such a secretory response was dramatically increased, and its shape modified, when glands were preperfused with K (17.7 mM)-Krebs: a peak of 3.77 +/- 0.42 micrograms 2 min-1 (n = 7) was reached at 18 min. This response was drastically reduced in the presence of nitrendipine (1 microM). 6. In summary, our results indicate that both [Na]0 reduction or Na accumulation into the chromaffin cell by inhibition of the Na pump with ouabain, greatly enhance the secretory efficacy of small increments of [K]0, and suggest that sodium may play a role in the regulation of catecholamine release mediated by voltage-dependent Ca channels in adrenal glands.