{'fraction_non_alphanumeric': 0.04667124227865477, 'fraction_numerical': 0.015099519560741249, 'mean_word_length': 5.075, '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}}
Modulation of Norepinephrine Release Through α1 and α2-Adrenoceptors in Rat Isolated Kidney

The aim of this study was to investigate α-adrenoceptor modulation of norepinephrine (NE) release from sympathetic nerves in rat isolated perfused kidney. After preincubation with [3H]NE, the renal nerves were stimulated. The stimulation-induced (S-I) outflow of radioactivity was used as an index of NE release. Clonidine (0.1 μmol/L) decreased the S-I outflow of radioactivity. This effect was abolished by the α1-adrenoceptor antagonist idazoxan (0.1 (μmol/L) but not by the α2-adreno-ceptor antagonist prazosin (0.1 μmol/L). Methoxamine (10 μmol/L) also had an inhibitory effect; this was abolished by prazosin (0.1 μmol/L), but not by idazoxan. Individually, these a-blocking drugs and the α1-adrenoceptor antagonist corynanthine (0.3 μmol/L) enhanced S-I outflow of radioactivity. In the presence of indomethacin (10 μmol/L), the inhibitory effect of methoxamine was abolished but clonidine still inhibited S-I outflow of radioactivity. The facilitatory effect of prazosin was also unaltered by indomethacin. These results suggest the existence of inhibitory prejunctional α1- and α2-adreno-ceptors in the kidney. The inhibitory effect of methoxamine seems to be mediated through prostaglandin inhibition of NE release. However, the evidence for inhibitory prejunctional a,-adrenoceptors rests solely on the facilitatory effects of prazosin and corynanthine.