Beta agonist regulation of sodium transport in fetal lung epithelium: roles of cell volume, cytosolic chloride and protein tyrosine kinase.
10.3346/jkms.2000.15.S.S42
- Author:
Yoshinori MARUNAKA
1
;
Naomi NIISATO
;
Yasushi ITO
Author Information
1. Department of Physiology, Kyoto Prefectural University of Medicine, Japan. marunaka@phys.kpu-m.ac.jp
- Publication Type:Research Support, Non-U.S. Gov't
- Keywords:
cAMP;
Tyrosine Phosphorylation;
Protein Kinase A;
Protein Tyrosine Kinase;
Alveolar Epithelium
- MeSH:
Adrenergic beta-Agonists/pharmacology*;
Animal;
Biological Transport/physiology;
Biological Transport/drug effects;
Cell Size/physiology;
Chlorides/metabolism*;
Cyclic AMP/metabolism;
Cytosol/metabolism;
Enzyme Inhibitors/pharmacology;
Female;
Fetus/cytology;
Forskolin/pharmacology;
Nitrobenzoates/pharmacology;
Pregnancy;
Protein-Tyrosine Kinase/metabolism*;
Rats;
Rats, Wistar;
Respiratory Mucosa/enzymology*;
Respiratory Mucosa/embryology;
Respiratory Mucosa/cytology;
Sodium/metabolism*;
Tyrphostins/pharmacology
- From:Journal of Korean Medical Science
2000;15(Suppl):S42-S43
- CountryRepublic of Korea
- Language:English
-
Abstract:
1) A beta agonist stimulated Na+ transport and decreased the intracellular Cl concentration ([Cl]c) associated with cell shrinkage via an increase in cytosolic cAMP level by activating adenylate cyclase in rat fetal distal lung epithelial (FDLE) cells. 2) Lowering [Cl-]c activated a 28-pS nonselective cation (NSC) channel by elongating the open time of the channel. 3) cAMP signals were converted to a protein tyrosine kinase (PTK)-mediated signal. 4) The PTK-mediated signal was involved in the cAMP-stimulated Na+ transport in rat FDLE cells.
