Release of [3H]noradrenaline from perfused rat hearts by potassium and its modifications by 6-hydroxydopamine and reserpine

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Abstract
The sources of noradrenaline (NA) released by excess K from isolated perfused rat hearts were investigated by labelling the hearts from normal, reserpine-treated and 6-hydroxydopamine-treated (6-OHDA-treated) rats with [3H]NA, and measuring the increased rate of efflux induced by perfusion with a Krebs solution containing varying amounts of excess K. The [3H]NA and its metabolites in the effluent were separated by adsorption on alumina and a cation-exchange resin (Dowex-50). The release induced by K was a linear function of the log of the increased K concentration. Following a 1 h efflux period after labelling with [3H]NA, the hearts from reserpine-treated rats retained 1/5 as much [3H]NA and released, in response to a 56 mM elevation in the K concentration, less than 1/6 as much tritium label as the hearts from untreated (control) animals. In contrast, the hearts from 6-OHDA-treated animals retained 1/15 of the amount of [3H]NA and released 1/50 of the 3H label as did the control hearts. The K induced increase of 3H-labeled substances in the effluent from the control hearts showed a large (3-fold) percentage increase in the [3H]NA fraction; the effluents from the hearts of reserpine-and 6-OHDA-treated animals contained only small increases in the [3H]NA fraction. Based on the assumptions that reserpine prevented retention of NA in the storage granules whereas 6-OHDA prevented almost all neuronal storage. More than 80% of the NA released by K excess from perfused normal hearts originated from the storage vesicles of the nerves, the remainder being largely from the cytoplasm of the nerves, with only a small portion from extraneuronal sources.