{'fraction_non_alphanumeric': 0.056228373702422146, 'fraction_numerical': 0.01124567474048443, 'mean_word_length': 5.969879518072289, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Mechanism of efflux of noradrenaline from adrenergic nerves in rabbit atria

1 The mechanism of efflux of (—)‐[3H]‐noradrenaline was examined in rabbit atria, which were pretreated with reserpine and pargyline. 2 Between 40 and 100 min, efflux occurred predominantly from a single intraneuronal compartment. 3 Efflux was rapidy increased by (—)‐ and (+)‐noradrenaline, tyramine and (±)‐metaraminol, but not by (±)‐isopropylnoradrenaline or (±)‐normetanephrine. The increase in efflux produced by (—)‐noradrenaline was inhibited by cocaine and desipramine but not by lidocaine. 4 Spontaneous effluxes, and those accelerated by (—)‐noradrenaline, were temperature‐sensitive. 5 Efflux was increased by ouabain, omission of K+, metabolic inhibition and lowering of the external Na+ concentration. These effects were significantly reduced by cocaine and desipramine but not by lidocaine. 6 These findings provide evidence that the efflux of [3H]‐noradrenaline from adrenergic nerves occurs by a cocaine‐sensitive, carrier‐mediated process. The characteristics of the efflux process are compatible with, but not conclusive proof for, the Na+‐gradient hypothesis.