Role of 5-hydroxytryptamine3 receptor antagonists in protecting pressure overload-induced cardiac hypertrophy in rats
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Role of 5-hydroxytryptamine3 receptor antagonists in protecting pressure overload-induced cardiac hypertrophy in rats
Journal of Chongqing Medical UniversityVol. 36, Issue 9, Pages: 1027-1031(2013)
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新疆医科大学附属中医医院心内二科,乌鲁木齐,830000
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Published:2013,
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WU Gang, CHENG Lu. Role of 5-hydroxytryptamine3 receptor antagonists in protecting pressure overload-induced cardiac hypertrophy in rats. [J]. Journal of Chongqing Medical University 36(9):1027-1031(2013)
DOI:
WU Gang, CHENG Lu. Role of 5-hydroxytryptamine3 receptor antagonists in protecting pressure overload-induced cardiac hypertrophy in rats. [J]. Journal of Chongqing Medical University 36(9):1027-1031(2013)DOI:
Role of 5-hydroxytryptamine3 receptor antagonists in protecting pressure overload-induced cardiac hypertrophy in rats
Objective:To discuss the role of 5-hydroxytryptamine3(5-HT3) receptor antagonist in the prevention of pressure overload induced myocardial hypertrophy. Methods:Thirty-two Kunming mice were randomly divided into four groups:sham-operation group(n=8),transverse aortic constriction(TAC) group(n=8),TAC + ondansetron(Ond) group(n=8) and TAC + tropisetron(Tro) group(n=8). TAC operation was performed and Ond and Tro intervene was followed on 3 d postoperatively. Rats were killed 4 weeks later and their body weight,heart weight,left heart weight,heart/weight ratio and left ventricular/weight ratio were measured and counted. Plasma norepinephrine(NE) levels were detected and heart pathological Masson staining was conducted. Eighteen Kunming mice were randomly divided into control group(n=6),Tro group(n=6) and Ond group(n=6). TAC operation was not performed and changes in plasma NE levels were observed. Results:Ond and Tro reduced the elevated plasma NE levels in mice with cardiac hypertrophy(F=7.96,P=0.001). Ond and Tro exerted postive effect on pressure ouerload induced myocardial hypertrophy. Conclusions:5-HT3 receptor antagonists can protect cardiac hypertrophy and restore desensitization of cardiac adrenergic responsiveness,the mechanism of which may be through reducing the sympathetic activity.