Dehydroepiandrosterone (DHEA) prevents and reverses chronic hypoxic pulmonary hypertension
| العنوان: | Dehydroepiandrosterone (DHEA) prevents and reverses chronic hypoxic pulmonary hypertension |
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| المؤلفون: | Michael Fayon, Etienne-Emile Baulieu, Pierre Dos Santos, Eric Dumas-de-La-Roque, Roger Marthan, Sébastien Bonnet, Hugues Begueret, Jean-Pierre Savineau |
| المصدر: | Proceedings of the National Academy of Sciences. 100:9488-9493 |
| بيانات النشر: | Proceedings of the National Academy of Sciences, 2003. |
| سنة النشر: | 2003 |
| مصطلحات موضوعية: | Male, medicine.medical_specialty, Potassium Channels, Hypertension, Pulmonary, Blotting, Western, Administration, Oral, Dehydroepiandrosterone, Muscle hypertrophy, Adjuvants, Immunologic, medicine.artery, Internal medicine, Pressure, medicine, Animals, Rats, Wistar, Hypoxia, Lung, Calcium metabolism, Multidisciplinary, Dose-Response Relationship, Drug, Voltage-dependent calcium channel, business.industry, Myocardium, Hemodynamics, Biological Sciences, Hypoxia (medical), medicine.disease, Myocardial Contraction, Pulmonary hypertension, Potassium channel, Rats, Endocrinology, Echocardiography, Pulmonary artery, Calcium, Calcium Channels, medicine.symptom, business, Oxidation-Reduction, hormones, hormone substitutes, and hormone antagonists |
| الوصف: | Pulmonary artery (PA) hypertension was studied in a chronic hypoxic-pulmonary hypertension model (7–21 days) in the rat. Increase in PA pressure (measured by catheterism), cardiac right ventricle hypertrophy (determined by echocardiography), and PA remodeling (evaluated by histology) were almost entirely prevented after oral dehydroepiandrosterone (DHEA) administration (30 mg/kg every alternate day). Furthermore, in hypertensive rats, oral administration, or intravascular injection (into the jugular vein) of DHEA rapidly decreased PA hypertension. In PA smooth muscle cells, DHEA reduced the level of intracellular calcium (measured by microspectrofluorimetry). The effect of DHEA appears to involve a large conductance Ca 2+ -activated potassium channel (BK Ca )-dependent stimulatory mechanism, at both function and expression levels (isometric contraction and Western blot), via a redox-dependent pathway. Voltage-gated potassium (Kv) channels also may be involved because the antagonist 4-amino-pyridine blocked part of the DHEA effect. The possible pathophysiological and therapeutic significance of the results is discussed. |
| تدمد: | 1091-6490 0027-8424 |
| الوصول الحر: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::72948af12b380376dc253ac2fd956df2Test https://doi.org/10.1073/pnas.1633724100Test |
| حقوق: | OPEN |
| رقم الانضمام: | edsair.doi.dedup.....72948af12b380376dc253ac2fd956df2 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 10916490 00278424 |
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