Adenosine and maximum coronary vasodilation in humans: myth and misconceptions in the assessment of coronary reserve

Excerpt

In the heart, the purine nucleoside adenosine acts on heart rate, contractile function and coronary blood flow. Adenosine acts as a negative chronotrope in the sinoatrial and atrioventricular nodes and in atrial myocytes through adenosine A₁ receptor activation [43, 45]. Adenosine acts as a negative inotrope, largely through its anti-adrenergic action after adenosine A₁ receptor activation [43]. Adenosine acts as a coronary dilator, largely through activation of adenosine A_2A receptors [43, 45]. In humans, arteriolar dilation in response to adenosine is mediated by A_2A receptors, adenylate cyclase and calcium-activated potassium channels in vascular smooth muscle cells [52]. Also, indirect effects contribute to the role of adenosine in coronary blood flow: adenosine inhibits presynaptic release of norepinephrine from sympathetic nerves [43], inhibits platelet aggregation [35] and inhibits leukocyte adherence to the vascular wall [59]. A₁ receptors are coupled to G_i/o proteins and their activation decreases cAMP, whereas A_2A receptors are coupled to G_s proteins and mediate an increase in cAMP [1, 43]. …