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Beta‐agonist‐induced activation of Na+ absorption and KCl release in rat fetal distal lung epithelium: a study of cell volume regulation
Author(s) -
Nakahari T,
Marunaka Y
Publication year - 1997
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1997.sp004044
Subject(s) - terbutaline , chemistry , agonist , biophysics , endocrinology , medicine , pharmacology , biochemistry , receptor , biology , asthma
The effects of terbutaline (a selective beta 2‐adrenoceptor agonist) on cell volume and ion transport in rat fetal distal lung epithelial (FDLE) cells were studied. In FDLE cells, benzamil (1 microM) induced cell shrinkage, while cell volume was increased by 1 mM quinine or 2 mM Ba2+ but was not affected by 5‐nitro‐2‐(3‐phenylpropylamino)‐benzoic acid (NPPB, 20 microM). Terbutaline (10 nM) induced transient cell swelling, which was suppressed by benzamil, while 10 microM terbutaline induced initial rapid cell shrinkage followed by delayed slow cell shrinkage, which was suppressed by 1 mM quinine or 20 microM NPPB but not by 2 mM Ba2+. Application of benzamil enhanced the cell shrinkage induced by 10 microM terbutaline. These observations suggest that: (1) benzamil‐blockable Na(+)ࢤpermeable channels and quinine‐ and Ba(2+)ࢤblockable K+ channels contribute to maintenance of cell volume of FDLE cells; (2) terbutaline at both 10 nM and 10 microM activates benzamil‐blockable Na(+)ࢤpermeable channels; (3) quinine‐blockable K+ channels are activated by 10 microM terbutaline; and (4) NPPB‐blockable Cl‐ channels are responsible for Clࢤ movement in cell volume changes induced by terbutaline. The present study demonstrates that the cellular mechanisms of volume change induced by terbutaline are closely related to activation of Na+ absorption and KCl release.