THE EFFECT OF THE INHIBITION OF THE ENDOTHELIAL RELEASE OF NITRIC-OXIDE ON CORONARY REACTIVE HYPEREMIA IN THE ANESTHETIZED DOG

The effect of the inhibition of the endothelial release of nitric oxid e (NO) on the hyperaemia which follows a 10 s coronary occlusion was s tudied in anaesthetized dogs. Aortic blood pressure was kept constant during the experiments using an arterial reservoir connected with the femoral arteries. The blood flow in the left circumflex coronary arter y was recorded with an electromagnetic flow probe. A 10 s coronary occ lusion was performed before and after intracoronary infusion of Nitro- L-arginine (LNNA), at the dose of 100 mg in 20 min. The effect of LNNA in preventing the release of NO by the endothelium was demonstrated b y the reduced coronary hyperaemia which follows the intracoronary infu sion of acetylcholine. After LNNA the baseline coronary flow was not a ltered. Following the release of the coronary occlusion the peak ampli tude of the reactive hyperaemia was not significantly changed, while t he duration was reduced to almost a half of the control. The results s uggest that in the intact dog NO is not important in the regulation of the baseline coronary vasomotor tone. It may also be argued that the peak amplitude of the hyperaemia is not significantly affected by LNNA either because the inhibition of the release of nitric oxide is count eracted by a greater production of adenosine, or because a mechanism n ot affected by nitric oxide (e.g. a myogenic mechanism) is involved in the reactive hyperaemia. In contrast the reduction of the duration of the hyperaemia after the inhibitor may depend on a reduced effect of the shear stress of the blood on the endothelium during the reactive h yperaemia.