Sildenafil Limits Monocrotaline-Induced Pulmonary Hypertension in Rats through Suppression of Pulmonary Vascular Remodeling

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Title:	Sildenafil Limits Monocrotaline-Induced Pulmonary Hypertension in Rats through Suppression of Pulmonary Vascular Remodeling
Authors:	Chia-Hung Yen, PhD;Steve Leu, PhD;Yu-Chun Lin, PhD;Ying-Hsien Kao, PhD;Li-Teh Chang, PhD;Sarah Chua, MD;Morgan Fu, MD;Chiung-Jen Wu, MD;Cheuk-Kwan Sun, MD, PhD;Hon-Kan Yip, MD
Keywords:	monocrotaline;pulmonary arterial hypertension;sildenafil
Date:	2010-06
Issue Date:	2011-09-27T02:40:46Z (UTC)
Abstract:	We hypothesize that sildenafil attenuates pulmonary hypertension through suppressing pulmonary vascular remodeling. Thirty male adult Sprague-Dawley rats were randomized to receive saline injection (Group 1), subcutaneous monocrotaline (MCT) (60 mg/kg) (Group 2), and MCT plus oral sildenafil (30 g/kg per day) (Group 3) 5 days after MCTadministration. By Day 35, Western blot showed lower connexin43 and membranous protein kinase C epsilon expressions but higher oxidative stress in right ventricle in Group 2 compared with the other groups. Additionally, pulmonary Smad1/5 was lowest, whereas connexin43 and Smad3 were highest in Group 2. Pulmonary mRNA expressions of tumor necrosis factor-a, caspase-3, plasminogen activator inhibitor-1, and transforming growth factor-b were higher, whereas bone morphogenetic protein Type II receptor, Bcl-2, and endothelial nitric oxide synthasewere lower in Group 2 than in the other groups. Similarly, mRNA expressions of tumor necrosis factor-a, caspase-3, andb-myosin heavy chainwere increased, whereas Bcl-2, endothelial nitric oxide synthase, and a-myosin heavy chain expressions in right ventricle were reduced in Group 2 compared with the other groups. Number of lung arterioles was lowest, whereas number of arterioles with muscularization of the medial layer was highest in Group 2. Right ventricle systolic pressure and weight were elevated in Group 2 compared with the other groups. In conclusion, sildenafil effectively alleviates MCT-induced pulmonary hypertension through suppressing pulmonary vascular remodeling.
Relation:	J Cardiovasc PharmacolTM 2010;55:574–584
Appears in Collections:	[Department of Nursing] Papers

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