| Fosinopril prevents the pulmonary arterial remodeling in sinoaortic-denervated rats by regulating phosphodiesterase. | |
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MedLine Citation:
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PMID: 18209565 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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AIM: To study the effects of fosinopril on sinoaortic denervation (SAD)-induced pulmonary vascular remodeling and on phosphodiesterases (PDE) 1 in rats. METHODS: SAD was performed in male Sprague-Dawley rats at the age of 10 weeks. The experiment included sham-operated (Sham), SAD, and fosinopril-treated SAD groups. Fosinopril (15 mg/kg/d) was given in rat chow. After 16 weeks of treatment, the pulmonary arteries were taken for investigations, including pharmacological study, measurement of cGMP, light microscopy, immunohistochemistry, Western blotting, and quantitative real-time RT-PCR. RESULTS: Compared with Sham rats, blood pressure variability (BPV) was significantly increased in the SAD group. However, the mean pulmonary artery pressure (mPAP) was not significant change among 3 groups. After SAD, maximal contraction of pulmonary artery rings to phenylephrine was markedly decreased; the most prominent morphological change in the lung included thickening vascular walls, increasing number of smooth muscle cells, and greater wall-to-lumen ratio; the tissue concentrations of cGMP was reduced significantly; PDE1A or PDE1C expression was upregulated significantly, and endothelial nitric oxide synthase (eNOS) expression was downregulated significantly. Fosinopril treatment prevented these changes induced by SAD. CONCLUSION: Pulmonary artery remodeling (structural and functional abnormalities) was induced by SAD. Fosinopril, an angiotensin-converting enzyme inhibitor, mainly via potentiating eNOS pathway and inhibiting AngII formation, effectively prevented increased blood pressure variability and vascular remodeling of the pulmonary artery after SAD by regulating the activity levels or expression of eNOS, cGMP, and PDE1s. |
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Authors:
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Xia Tao; Ya-Jun Zhang; Fu-Ming Shen; Yun-Feng Guan; Ding-Feng Su |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cardiovascular pharmacology Volume: 51 ISSN: 0160-2446 ISO Abbreviation: J. Cardiovasc. Pharmacol. Publication Date: 2008 Jan |
Date Detail:
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Created Date: 2008-01-22 Completed Date: 2008-04-03 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7902492 Medline TA: J Cardiovasc Pharmacol Country: United States |
Other Details:
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Languages: eng Pagination: 24-31 Citation Subset: IM |
Affiliation:
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Department of Pharmacy, Changzheng Hospital, Second Military Medical University, Shanghai, China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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drug effects,
metabolism Angiotensin-Converting Enzyme Inhibitors / pharmacology Animals Antihypertensive Agents / pharmacology* Baroreflex Blood Pressure / drug effects* Cyclic GMP / metabolism Denervation Fosinopril / pharmacology* Gene Expression Regulation / drug effects Male Nitric Oxide Synthase Type III / drug effects, metabolism Phosphoric Diester Hydrolases / drug effects*, metabolism Pulmonary Artery / drug effects*, pathology Rats Rats, Sprague-Dawley |
| Chemical | |
Reg. No./Substance:
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0/Angiotensin-Converting Enzyme Inhibitors; 0/Antihypertensive Agents; 11128-99-7/Angiotensin II; 7665-99-8/Cyclic GMP; 98048-97-6/Fosinopril; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 3.1.4.-/Phosphoric Diester Hydrolases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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