{'fraction_non_alphanumeric': 0.029156816390858944, 'fraction_numerical': 0.002364066193853428, 'mean_word_length': 5.2254901960784315, '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}}
beta-Adrenoceptor activates endothelium-dependent release of nitric oxide in rat aorta.

AIM
To examine the possible role of agents elevating cAMP to release NO from aortic endothelial cells.


METHODS
NG-nitro-L-arg inine methylester (L-NAME), an inhibitor of NO synthase, partially inhibited endothelium-dependent relaxation evoked in phenylephrine-precontracted rings by isoproterenol and abolished relaxation mediated by forskolin 0.2 mumol L-1.


RESULTS
In rings without endothelium, isoproterenol and forskolin were less effective relaxants and L-NAME had no effect on the responses. In methylene blue-treated rings isoproterenol- and forskolin-induced relaxation were prevented in both endothelium-intact and -denuded rings, but the inhibitory effect of methylene blue were significantly more in rings with endothelium than in those without. On the other hand, relaxation induced by sodium nitroprusside was not inhibited by L-NAME, but was inhibited by methylene blue in both the endothelium-intact and -denuded rings. The concentration-relaxation curves to sodium nitroprusside after methylene blue were identical for rings with and without endothelium.


CONCLUSION
beta-Adrenoceptors or any agent which raises cAMP elevate NO release from endothelial cells.