title: Hydrogen sulfide attenuates cardiac hypertrophy and fibrosis induced             by abdominal aortic coarctation in rats.
abstract: Hydrogen sulfide (H2S) has been recently found to be an endogenous signaling             gasotransmitter. Cardiac hypertrophy often develops in the course of heart failure.             It is unknown whether or not endogenous H2S protects cardiac hypertrophy. This             study was conducted to examine the effects of H2S on cardiac hypertrophy and fibrosis             induced by abdominal aortic coarctation and to explore its mechanisms. Male Sprague-Dawley             rats were randomly divided into five groups: normal, sham, abdominal aortic coarctation             (AAC), AAC treated with enalapril and AAC treated with H2S. One week after surgery,             enalapril and sodium hydrosulfide (NaHS)-treated rats were fed for 28 consecutive             days and sacrificed. After that, the left ventricle mass index (LVMI), cardiomyocyte             size and areas, collagen volume fraction (CVF) of the rats were measured. In the             AAC rats, the LVMI, the cardiomyocyte size and areas, and the CVF were all markedly             increased while in the H2S groups they were significantly reduced. H2S decreased             the levels of Ang-II in the heart, but not in plasma. In addition, H2S also improved             the expression of connexin 43 (Cx43). Our results suggest that H2S can significantly             suppress cardiac hypertrophy and fibrosis induced by overloaded pressure, possibly             by inhibiting the activity of intracardiac Ang-II and by modifying expression             of Cx43.
authors.affiliation: Department of Cardiology, Medical College, The First Affiliated Hospital of Shantou University, Shantou, Guangdong 515041, PR China.
authors.forename: Jinglong
authors.initials: J
authors.lastname: Huang
authors.forename: Dongming
authors.initials: D
authors.lastname: Wang
authors.forename: Jinbin
authors.initials: J
authors.lastname: Zheng
authors.forename: Xiansheng
authors.initials: X
authors.lastname: Huang
authors.forename: Hong
authors.initials: H
authors.lastname: Jin
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology / Q000627:therapeutic use; D001017:Aortic Coarctation; D006332:Cardiomegaly / Q000188:drug therapy* / Q000473:pathology; D018031:Connexin 43 / Q000378:metabolism; D004656:Enalapril / Q000494:pharmacology / Q000627:therapeutic use; D005355:Fibrosis / Q000188:drug therapy* / Q000473:pathology; D006862:Hydrogen Sulfide / Q000494:pharmacology / Q000627:therapeutic use*; D008297:Male; D032383:Myocytes, Cardiac / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000959:Antihypertensive Agents; D018031:Connexin 43; D000804:Angiotensin II; D004656:Enalapril; D006862:Hydrogen Sulfide