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.