ANP inhibits surfactant secretion from isoproterenol stimulated alveolar type II cells.
- Author:
Young Man LEE
1
Author Information
1. Department of Physiology, School of Medicine Catholic University of University, Taegu-Hyosung, Taegu 705-034 South Korea.
- Publication Type:Original Article
- Keywords:
Alveolar type II cells;
Surfactant;
ARDS
- MeSH:
1-Methyl-3-isobutylxanthine;
Animals;
Anoxia;
Atrial Natriuretic Factor*;
Choline;
Estrogens, Conjugated (USP);
Heart;
Heart Failure;
Isoproterenol*;
Lung;
Pulmonary Edema;
Rats;
Respiratory Distress Syndrome, Adult
- From:The Korean Journal of Physiology and Pharmacology
1997;1(1):65-70
- CountryRepublic of Korea
- Language:English
-
Abstract:
In order to investigate the effect of ANP on surfactant secretion from alveolar type II cell(AT II cell) during circulatory derangement in adult respiratory distress syndrome (ARDS), the secretion of surfactant from AT II cells was evaluated in purely isolated AT II cultures from rat lungs. For the simulation of sympathetic stimulation during circulatory derangement, primary AT II cultures were incubated with isoproterenol and IBMX. In this isoproterenol stimulated AT II cells, ANP were added in the media for the investigation of effect of ANP on surfactant secretion from AT II cells. For the evaluation of surfactant secretion,(3H)-methylcholine was incorporated and the level of radiolabelled choline chloride secreted from the cells was determined. As previously reported, isoproterenol and IBMX stimulated surfactant secretion from AT II cells. Isoproterenol showed synergistic increase of surfactant secretion with IBMX in AT II cells. In isoproterenol stimulated AT II cells, physiological level of ANP inhibited the secretion of surfactant in primary cultures of AT II cells. On the basis of these experimental it is suggested that, in association with circulatory change during ARDS, increased secretion of ANP by the pulmonary edema, hypoxia and congestive heart heart failure might aggravate the symptoms of ARDS by reduction of surfactant secretion from AT II cells.
