Modulation of uptake2 of3H-(±)-isoprenaline by isoprenaline-induced depolarization of rat salivary gland cells

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Abstract
Previous observations by Almgren and Jonason (1974) showed that propranolol is able to increase the extraneuronal accumulation of3H-isoprenaline in rat salivary gland slices. The present experiments were carried out in order to test the hypothesis that3H-isoprenaline, by acting on beta-adrenoceptors, might depolarize the gland cells and thereby hinder its own uptake2 and that this hindrance might be prevented by propranolol. After inhibition of catechol-O-methyltransferase the extraneuronal accumulationof the3H-catecholamine in slices of rat salivary glands was determined subsequent to 20 min of exposure of the tissue to 0.5 to 5,000 nmol/l3H-(±)-isoprenaline. Expressed as a tissue/medium ratio, accumulation decreased with increasing amine concentration, although all amine concentrations were well below those saturating uptake2. The3H-isoprenaline-induced decrease of the tissue/medium ratio was antagonized by (−)-propranolol, and increasing concentrations of the antagonist were needed to antagonize the effect of increasing concentrations of3H-isoprenaline. In parallel experiments K+-induced (60 mmol/l) depolarization reduced the tissue/medium ratio observed for 0.5 nmol/l3H-(±)-isoprenaline. Gland slices were preloaded with3H-(±)-isoprenaline and then washed out for 60 min with solution not containing labelled amine. When 500 nmol/l(±)-isoprenaline were present in the wash-out solution, the addition of 10 μmol/l (−)-propranolol impeded the efflux of3H-isoprenaline. In parallel experiments. K+-induced (60 mmol/l) depolarization facilitated the efflux of3H-isoprenaline [in the presence of 10 μmol/l (−)-propranolol]. The results support the working hypothesis. They provide an explanation for the findings of Almgren and Jonason (1974); moreover, they indicate that the membrane potential is an important modulator of uptake2.

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