{'fraction_non_alphanumeric': 0.039525691699604744, 'fraction_numerical': 0.01383399209486166, 'mean_word_length': 5.102409638554217, '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}}
In vitro maturation of the rat reticulocyte beta-adrenoceptor adenylate cyclase system.

Reticulocytes but not mature erythrocytes are equipped with a functional beta-adrenergic system characterizing cells which are under adrenergic control. We have followed the decline of beta-adrenergic functions in a defined, phenylhydrazine-induced population of rat reticulocytes during maturation under cell culture conditions in vitro. beta-Agonist or forskolin-stimulated cyclic 3',5'-AMP (cAMP) formation decreased by 35 +/- 5% within 18 h and by 75 +/- 7% within 5 days. Regulatory control, i.e. the desensitization after chronic agonist exposure was observed at least for the first 18 h of incubation. The protein components of the system (receptors, nucleotide binding protein (N-protein), cyclase) seem to survive longer than 5 days. Our results suggest that an impaired interaction between N-protein and adenylate cyclase may be the initial step in the inactivation of the beta-adrenergic system in reticulocytes.