Regulation of lung edema clearance by dopamine

Yochai Adir, Jacob I Sznajder*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

14 Scopus citations

Abstract

In the kidney, dopamine inhibits Na,K-ATPase, which results in natriuresis because less Na+ is reaabsorbed by the proximal and distal tubules. In contrast, dopamine stimulates Na,K-ATPase activity in the alveolar epithelium, leading to increased alveolar fluid reabsorption. Importantly, dopamine increases alveolar fluid reabsorption not only in normal alveolar epithelium but also in models of lung injury. Dopamine short-term regulation of alveolar epithelial Na,K-ATPase occurs via D1 receptor activation, protein kinase C and protein phosphatase 2A pathways, leading to increased Na,K-ATPase activity by recruiting sodium pumps from the intracellular compartment to the basolateral membranes. Conversely, D2 receptor activation by long-term dopamine regulates (∼ 24 hours) alveolar epithelial Na,K-ATPase via the MAPK pathway, which results in de novo synthesis of Na,K-ATPase proteins. Conceivably, by increasing Na,K-ATPase activity and promoting alveolar fluid reabsorption, dopamine can be of clinical relevance for the treatment of patients with acute hypoxemic respiratory failure due to pulmonary edema.

Original languageEnglish (US)
Pages (from-to)47-50
Number of pages4
JournalIsrael Medical Association Journal
Volume5
Issue number1
StatePublished - Jan 1 2003

Keywords

  • Clearance
  • Dopamine
  • Edema
  • Lung

ASJC Scopus subject areas

  • Medicine(all)
  • Bioengineering

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