Adenine Sulfate Improves Cardiac Function and the Cardiac Cholinergic System After Myocardial Infarction in Rats

Journal of Pharmacological Sciences

Ke-Yu Ren²  Lei Sun²  Dong-Ling Li²  Jian-Kang Liu³  Xiao-Jiang Yu²  Wei-Jin Zang²  Xiao-Li Xu²  Bing Wang¹  Jun Lu² 

[1] Department of Pathology, College of Medicine, School of Life Science and Technology, Xi’an Jiaotong University, China;Department of Pharmacology, School of Life Science and Technology, Xi’an Jiaotong University, China;Institute of Mitochondrial Biology & Medicine, School of Life Science and Technology, Xi’an Jiaotong University, China

关键词: adenine sulfate;    cardioprotection;    muscarinic receptor;    nitric oxide;    myocardial infarction;   

DOI  :  10.1254/jphs.10231FP

学科分类：药学

来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society

【 摘 要 】

References(28)Cited-By(6)Recent studies have shown that vagal activation may have an important therapeutic implication for myocardial infarction (MI), but effective strategies remain unexplored. Here, we investigate whether adenine sulfate can preserve cardiac function and the cholinergic system against MI. Rats were treated with adenine sulfate for three weeks after coronary ligation. Cardiac function was assessed by hemodynamics. The muscarinic M2 receptor and cholinesterase-positive nerves were semi-quantified by immunochemical and histochemical staining. The maximal binding capacity (Bmax) of muscarinic receptors, determined by radioligand binding assay, showed that cardiac function was impaired in MI rats. Adenine sulfate reversed MI-induced reduction of mean artery pressure and left ventricular systolic pressure and elevation of left ventricular end-diastolic pressure. Moreover, adenine sulfate also increased nitric oxide (NO) and nitric oxide synthase (NOS) activity. The amelioration was accompanied by a reversal of the infarction-induced reduction of cholinesterase-positive nerves and M2-receptor expression and Bmax in the adenine sulfate high dose group. Meanwhile, adenine sulfate treatment corrected the disorder of cardiac redox state by reduction in maleic dialdehyde and increase in superoxide dismutase. In conclusion, adenine sulfate exerts cardioprotection against MI and ameliorates NO production. Changes in cardiac vagal distribution density and M2-receptor expression raise the possibility that improvement of the cardiac cholinergic system is involved in adenine sulfate–induced cardioprotective effects.

【 授权许可】

Unknown