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pubmed-article:736168pubmed:abstractTextRabbit lungs were perfused via the pulmonary artery and norepinephrine (NE) measured in the outflows. The basal NE level was approximately 3 ng/min. Electrical stimulation (50 V, 1 ms, 10 Hz) of the sympathetic nerves doubled the NE release. Hexamethonium (10(-4) and 10(-5) M) had no effect on the release of NE. Administration of a monoamine oxidase (MAO) inhibitor, pargyline (70 mg/kg) resulted in a 20-fold NE increase by nerve stimulation, implying that the bulk of the amine does not reach the systemic circulation due to an active MAO. Methacholine (1 and 10 micrograms/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 micrograms/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PGE2 (100 ng/ml), but not PGS2alpha, (100 ng/ml), depressed NE release during nerve stimulation, whereas indomethacin (10 mg/kg) enhanced NE release before, during, and after nerve stimulation in seemingly normal animals. This indicates the existence of another presynaptic inhibitory mechanism for NE release in the lung: a PGE-mediated inhibition.lld:pubmed
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pubmed-article:736168pubmed:articleTitleRelease of norepinephrine by sympathetic nerve stimulation from rabbit lungs.lld:pubmed
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pubmed-article:736168pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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