1. Hypoxic activation of an amiloride-sensitive cation conductance in alveolar epithelial cells.
- Author
-
Jovanovic S, Land SC, Olver RE, and Wilson SM
- Subjects
- Animals, Cell Hypoxia, Cell Line, Dexamethasone pharmacology, Electric Conductivity, Glucocorticoids pharmacology, Hormone Antagonists pharmacology, Hydrogen Peroxide metabolism, Ion Transport, Mifepristone pharmacology, Mitogen-Activated Protein Kinase 3, Mitogen-Activated Protein Kinases antagonists & inhibitors, Mitogen-Activated Protein Kinases metabolism, Oxidative Stress, Oxygen physiology, Pressure, Respiratory Mucosa drug effects, Amiloride pharmacology, Pulmonary Alveoli cytology, Respiratory Mucosa physiology, Sodium metabolism
- Abstract
Imposing hypoxia (P(O(2)) = 23 mmHg) upon A549 cells elicited increased G(amil) although previous work had predicted a fall in this parameter. G(amil) appeared to be dependent upon glucocorticoid-driven gene expression, a process inhibited by ERK, an enzyme activated by oxidative stress. However, hypoxia transiently activated this enzyme and the response was blocked by glucocorticoids, showing that the rise in G(amil) occurs only if ERK activation is suppressed. Fluorimetric assays showed that lowering P(O(2)) elicited H(2)O(2) formation indicating that this maneuver actually imposes oxidative stress, thus explaining how hypoxia can elicit responses normally associated with a rise in P(O(2))., (Copyright 2001 Academic Press.)
- Published
- 2001
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