Hypoxia preadaptation prevents oxygen-induced depression of lung angiotensin-converting enzyme activity

Robert Jackson, J. B. Pisarello

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

Preadaptation of adult rats to hypoxia (10% O2 for 5 days) results in tolerance to oxygen-induced lung injury (> 95% O2 for 2 days). This study investigated whether hypoxia preadaptation maintained an endothelial cell metabolic function, angiotensin-converting enzyme (ACE) activity, despite exposure to hyperoxia. Lung ACE activity was measured as the capacity of isolated, ventilated, perfused lungs to hydrolyze an ACE substrate, benzoyl-phenylalanyl-alanyl-proline (BPAP), after in vivo hypoxia, hyperoxia, or sequential hypoxia-hyperoxia exposure. The results indicated that (1) hyperoxia decreases BPAP hydrolysis in isolated lungs, (2) hypoxia preadaptation does not affect BPAP hydrolysis [measured at ambient P(O2)], and (3) hypoxia preadaptation prevents hyperoxia-induced depression of lung ACE activity. These data imply that lung microvascular endothelial cells participate in the development of oxygen tolerance in this model.

Original languageEnglish
Pages (from-to)424-428
Number of pages5
JournalAmerican Review of Respiratory Disease
Volume130
Issue number3
StatePublished - Jan 1 1984
Externally publishedYes

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Peptidyl-Dipeptidase A
Hyperoxia
Oxygen
Lung
Proline
Hydrolysis
Endothelial Cells
Lung Injury
Hypoxia

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

Cite this

Hypoxia preadaptation prevents oxygen-induced depression of lung angiotensin-converting enzyme activity. / Jackson, Robert; Pisarello, J. B.

In: American Review of Respiratory Disease, Vol. 130, No. 3, 01.01.1984, p. 424-428.

Research output: Contribution to journalArticle

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