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Normobaric hypoxia stimulates endothelin-1 gene expression in the rat
T S Elton1, S Oparil, G R Taylor
1Department of Medicine, University of Alabama, Birmingham 35294.
The American Journal of Physiology
|December 1, 1992
Summary
Hypoxia significantly increases circulating endothelin-1 (ET-1) levels in rats, primarily originating from the lungs. This suggests ET-1 plays a role in hypoxic pulmonary hypertension.
Area of Science:
- Cardiovascular Physiology
- Respiratory Medicine
- Molecular Biology
Background:
- Endothelin-1 (ET-1) is a potent vasoconstrictor peptide.
- Hypoxia is known to affect cardiovascular function.
- The role of ET-1 in hypoxia-induced cardiovascular changes requires further elucidation.
Purpose of the Study:
- To investigate the effect of hypoxia on ET-1 gene expression and circulating levels in rats.
- To determine the primary source of hypoxia-induced ET-1 elevation.
Main Methods:
- Rats were exposed to normobaric hypoxia (10% O2) or room air for 24 or 48 hours.
- Arterial ET-1 levels were measured using radioimmunoassay.
- ET-1 mRNA levels in various tissues were quantified via slot blot hybridization using a specific rat prepro ET-1 cDNA probe.
Main Results:
- Circulating ET-1 levels were significantly elevated at 24 and 48 hours of hypoxia compared to controls.
- ET-1 mRNA levels showed a significant 2-fold increase in the lung and right atrium after 48 hours of hypoxia.
- No significant changes in ET-1 mRNA were observed in organs of the systemic vascular bed.
Conclusions:
- Hypoxia exposure leads to increased circulating ET-1 levels in rats.
- The primary source of hypoxia-induced ET-1 is likely pulmonary.
- Pulmonary ET-1 production may contribute to the development of hypoxic pulmonary hypertension through paracrine mechanisms.