[Expression of endothelin-1 mRNA, endothelin receptor-A and nitric oxide synthase mRNA in pulmonary artery and right ventriculus cordis of rats exposed to hypoxia]
- PMID: 7584571
[Expression of endothelin-1 mRNA, endothelin receptor-A and nitric oxide synthase mRNA in pulmonary artery and right ventriculus cordis of rats exposed to hypoxia]
Abstract
Endothelins (ETs) are a family of novel regulatory peptides which can constrict the vascular and promote the proliferation of vascular smooth muscle cells. Serum ET-1 was elevated, and nitric oxide (NO) levels were reduced in hypoxic pulmonary hypertension. However, the exact mechanism remains unclear, and no study has elucidated if hypoxia could stimulate directly overgrowth of right ventricle in patients with chronic cor pulmonale. To investigate the role of ET-1 and NO in hypoxia-induced pulmonary hypertension and right ventricular hypertrophy, we measured the levels of ET-1 mRNA, ET receptor-A (ETR-A) mRNA and nitric oxide synthase (NOS) mRNA in the pulmonary artery and right ventricle of rats exposed to hypoxia (FiO = 0.1, 8 hours daily for 1, 2 and 3 weeks) by reverse transcription-polymerase chain reaction (RT-PCR). ET-1 mRNA level of pulmonary artery raised after 1 week's hypoxia (P < 0.05), and after 2 weeks' hypoxia, it returned to near normal, but elevated significantly again after 3 weeks' hypoxia. Pulmonary artery ETR-A mRNA in 1 and 2 weeks hypoxic groups showed no significant change, but it raised significantly in 3 weeks' hypoxic group. After exposure to hypoxia for 1, 2 and 3 weeks, NOS mRNA in the pulmonary artery all reduced significantly (P < 0.05). The right ventriculus cordis showed a significant increase in weight after 3 and 2 weeks' hypoxia. ET-1 mRNA showed no significant change but ETR-A mRNA increased significantly after 2 weeks' hypoxia; both ET-1 mRNA and ETR-A mRNA showed significant increase in weight after 3 and 2 weeks' hypoxia. In the ventriculus cordis of rats exposed to hypoxia for 2 and 3 weeks, NOS mRNA had no significant change.
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