Our results indicated that (a) EA at PC6 has better effect than EA at LI6 and sham acupoint in affecting RPP and ECG, increasing ATP and ADO production, decreasing AMP production, and upregulating the expression levels of A1AR, A2aAR, and A2bAR; (b) A1AR and A2bAR are involved in EA-induced cardio protection in MI injury; and (c) silence of A1AR or A2bAR reverses the influence of EA at PC6 in upregulating the other two adenosine receptors and silence of A2aAR has no influence on the effect of EA at PC6 in upregulating A1AR and A2bAR. This evidence concerns the gene ADO and myocardial infarction.