Enhanced endothelin-1 and endothelin receptor gene expression in chronic hypoxia
Autor: | Qing Cheng Meng, T. S. Elton, Huaibin Li, Suzanne Oparil, Joan Durand, Shi-Juan Chen, Yiu-Fai Chen |
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Rok vydání: | 1994 |
Předmět: |
Male
medicine.medical_specialty Physiology Hypertension Pulmonary Molecular Sequence Data Gene Expression Aorta Thoracic Rats Sprague-Dawley Oxygen Consumption Physiology (medical) medicine.artery Internal medicine Animals Medicine Thoracic aorta Pulmonary Wedge Pressure RNA Messenger Hypoxia Receptor Aorta Lung Base Sequence Receptors Endothelin business.industry Endothelins Myocardium respiratory system medicine.disease Pulmonary hypertension Endothelin 1 Rats Endocrinology medicine.anatomical_structure Chronic Disease Pulmonary artery cardiovascular system DNA Probes business Endothelin receptor |
Zdroj: | Journal of Applied Physiology. 77:1451-1459 |
ISSN: | 1522-1601 8750-7587 |
Popis: | To test the hypothesis that endothelin (ET)-1 synthesis and ET receptor levels are increased selectively in the lung of rats with chronic hypoxic pulmonary hypertension, the current study examined the effects of exposure to chronic hypoxia (10% O2, 1 atm, 4 wk) on pulmonary arterial pressure, ET-1 levels in plasma and lung, and ET-1 and ETA and ETB receptor mRNA levels in lung, heart, pulmonary artery, aorta, kidney, spleen, and liver. Hypoxic exposure was associated with increases in pulmonary arterial pressure, plasma ET-1 levels, ET-1 mRNA in lung and pulmonary artery, and ET-1 stores and ETA and ETB receptor mRNA levels in lung. In thoracic aorta and the four heart chambers, ETA and ETB receptor mRNA levels were increased, but ET-1 mRNA levels were unchanged from air control levels. No change in ET-1 or ET receptor mRNA levels was seen in organs perfused by the systemic vascular bed, except in liver, where ETA receptor mRNA levels were decreased. The findings of concomitant increases in gene transcript levels for ET-1 and the ETA and ETB receptors in lung, but not in the great vessels or any other organ examined, are consistent with the hypothesis that increased ET-1 synthesis in the lung contributes to pulmonary vascular remodeling and the maintenance of chronic hypoxic pulmonary hypertension. |
Databáze: | OpenAIRE |
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