6533b7d1fe1ef96bd125ccae

RESEARCH PRODUCT

The neuronal efflux of noradrenaline: Dependency on sodium and facilitation by ouabain

subject

description

Rabbit hearts were isolated after pretreatment with the MAO inhibitor pargyline and with reserpine and were perfused with 200 ng/ml noradrenaline for 1 h. During the subsequent wash-out with an amine-free solution for 2 h, the neuronal efflux of noradrenaline declined mono-exponentially with a mean halftime of 42 min. Both Na+-free solution and ouabain caused facilitation of the efflux which thereafter declined in a multi-exponential fashion. The maximum facilitation was reached after 3 min of Na+-free perfusion and 25 min after introduction of ouabain. The amount of exogenous noradrenaline accumulated in the heart was only partially released when the extracellular Na+-concentration was normal, whereas perfusion with low Na+-solution evoked a complete release of the accumulated noradrenaline. In conclusion, the noradrenaline leaving the adrenergic neurone with the neuronal efflux originates preferentially in one intraneuronal compartment, when the external Na+-concentration is normal. Reduction of external Na+-concentration, however, seems to evoke the release from multiple intraneuronal compartments in series. The effect of Na+-depletion can be explained by the Na+-gradient hypothesis, but evidence is still lacking. The normal Na+-gradient seems to serve as a prerequisite for the axoplasmic retention of noradrenaline under the present conditions.