NO and adenosine both fit as the probable candidates. However, single best response would be adenosine, and NO could be taken as the mediator of the adenosine action. As per the Berne's hypothesis: When myocardial O2 demand increases (as during increased hea rate) -> increased breakdown of ATP in the myocardial cells -> ATP conveed to ADP, AMP, and finally adenosine -> adenosine leaks out of the cells, reaches the vessels, and causes vasodilation & increases blood flow. At low concentrations ~ adenosine acts the release of NO At higher concentrations ~ adenosine acts directly on the ATP-sensitive K+ channels in the VSMC of the coronary vessels.