Further evidence for the role of adenosine in hypercapnia/acidosis-evoked coronary flow regulation

Experiments were performed on isolated, nonworking rat hearts perfused at c onstant pressure according to the Langendorff technique to evaluate the rol e of adenosine in hypercapnia-evoked coronary vasodilation. Hypercapnia/aci dosios resulted in increases in heart rate and coronary flow rates in conju nction with a decrease in ventricular contractile tensions. The adenosine d eaminase inhibitor erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA, 10 mu M) re duced the heart rate and enhanced CO2-evoked increases in coronary vascular flow. 5-Iodotubercidin (1 mu M), an inhibitor of adenosine kinase, caused a reduction in heart rate and enhanced coronary flow rates during hypercapn ic perfusion. Adenosine deaminase (1 U/ml) significantly attenuated CO2-evo ked increases in coronary vascular flow. These results extend those of prev ious investigations implicating adenosine in the regulation of coronary flo w during conditions of respiratory or metabolic acidosis. (C) 1999 Elsevier Science Inc. All rights reserved.