We previously reported that lung edema clearance was stimulated by dopamine (DA). The purpose of this study was to determine whether the DA- mediated stimulation of edema clearance occurs via an adrenergic or dopaminergic regulation of alveolar epithelial Na, K-ATPase. When isolated perfused rat lungs were coinstilled with DA and SCH 23390 (a specific D1 receptor antagonist), there was a dose-dependent attenuation of the stimulatory effects of DA. Coinstillation with S-sulpiride (a specific D2 receptor antagonist) or propranolol (a β-adrenergic antagonist) did not alter DA-stimulated clearance. Similarly, the specific dopaminergic D1 agonist fenoldopam increased lung edema clearance, but quinpirole (a specific dopaminergic D2 agonist) did not. 125I-SCH 23982 binding studies suggested that D1 receptors are expressed on alveolar type II (ATII) cells with an apparent dissociation constant (K(d)) of 4.4 nM and binding maximum (Bmax) 9.8 pmol/mg. Consistent with these results, the D1 receptor messenger RNA (mRNA) and protein were detected in ATII cells by reverse transcriptase- polymerase chain reaction (RT-PCR) and Western blot analysis, respectively. These data demonstrate a novel mechanism involving the activation of dopaminergic D1 receptors which mediates DA-stimulated edema removal from rat lungs.
|Original language||English (US)|
|Number of pages||5|
|Journal||American journal of respiratory and critical care medicine|
|State||Published - 1999|
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
- Critical Care and Intensive Care Medicine