Release of norepinephrine by sympathetic nerve stimulation from rabbit lungs
- 1 December 1978
- journal article
- research article
- Published by American Physiological Society in American Journal of Physiology-Heart and Circulatory Physiology
- Vol. 235 (6) , H803-H808
- https://doi.org/10.1152/ajpheart.1978.235.6.h803
Abstract
Rabbit 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 .mu.g/ml) inhibited NE release by nerve stimulation. This inhibition was abolished by atropine (5 .mu.g/ml). It is suggested that a muscarinic inhibitory mechanism may regulate the NE release in the lung. PG[prostaglandin]E2 (100 ng/ml), but not PGF2.alpha., (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.This publication has 2 references indexed in Scilit: