{'fraction_non_alphanumeric': 0.04499274310595065, 'fraction_numerical': 0.01088534107402032, 'mean_word_length': 4.995652173913044, '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}}
Central inhibition of nitric oxide synthesis increases blood pressure and heart rate in anesthetized rats.

In the present study we evaluated the cardiovascular responses to inhibition of endogenous nitric oxide (NO) formation in the brain with intracerebroventricular (i.c.v) administration of N omega-nitro-L-arginine methyl ester (L-NAME), a specific inhibitor of NO synthase. L-NAME (30 micrograms and 300 micrograms i.c.v) induced a dose-dependent increase in mean arterial pressure and heart rate in anesthetized normotensive rats, while its enantiomer D-NAME (300 micrograms i.c.v.) increased blood pressure only slightly and transiently. The pressor response to L-NAME was partially attenuated by i.c.v. administration of NO precursor L-arginine (300 micrograms), whereas D-arginine, the stereoisomer which cannot serve as a percursor for the biosynthesis of NO, was ineffective. Inhibition of beta 1-adrenoceptors by pretreatment with atenolol (2.5 mg/kg i.v.) reduced the pressor and tachycardic effect of subsequently administered L-NAME, whereas muscarinic receptor antagonist methylatropine (2 mg/kg i.v.) did not affect the cardiovascular effects of L-NAME. These findings imply that the pressor response to i.c.v. L-NAME results from withdrawal of the inhibitory effect of endogenous NO on a central pressor mechanism which acts by increasing sympathetic outflow.