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Hydrogen sulfide (H2S) has been recently found to be an endogenous signalinggasotransmitter. Cardiac hypertrophy often develops in the course of heart failure.It is unknown whether or not endogenous H2S protects cardiac hypertrophy. Thisstudy was conducted to examine the effects of H2S on cardiac hypertrophy and fibrosisinduced by abdominal aortic coarctation and to explore its mechanisms. Male Sprague-Dawleyrats 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 consecutivedays and sacrificed. After that, the left ventricle mass index (LVMI), cardiomyocytesize and areas, collagen volume fraction (CVF) of the rats were measured. In theAAC rats, the LVMI, the cardiomyocyte size and areas, and the CVF were all markedlyincreased while in the H2S groups they were significantly reduced. H2S decreasedthe levels of Ang-II in the heart, but not in plasma. In addition, H2S also improvedthe expression of connexin 43 (Cx43). Our results suggest that H2S can significantlysuppress cardiac hypertrophy and fibrosis induced by overloaded pressure, possiblyby inhibiting the activity of intracardiac Ang-II and by modifying expressionof Cx43.

Hydrogen sulfide attenuates cardiac hypertrophy and fibrosis induced by abdominal aortic coarctation in rats