THE ROLE OF NITRIC-OXIDE IN THE INITIATION AND IN THE DURATION OF SOME VASODILATOR RESPONSES IN THE CORONARY CIRCULATION

In the coronary bed vasodilatation can be mediated by several mechanis ms including endothelium-produced nitric oxide. To examine the contrib ution of nitric oxide, three different techniques to cause vasodilatat ion in the coronary vessels were used in the anaesthetized dog: intrac oronary injection of 1 mu g acetylcholine, sudden reduction of the aor tic blood pressure inducing a myogenic response and transient occlusio n followed by release of the left circumflex coronary artery causing r eactive hyperaemia. Each manoeuvre was performed before and after intr acoronary adminstration of 100 mg N-nitro-L-arginine, an inhibitor of the synthesis of nitric oxide. In contrast to previous investigations, the inhibition of nitric oxide synthesis was prevented from causing a n increase in blood pressure by the use of a blood-pressure-compensati ng device. The results observed during each of the three techniques, s uggest that the initial cause of the vasodilatation is not the result of the increase of the production of nitric oxide. However, subsequent to the initiation of vasodilatation, an increase in the shear stress can result in an increase in the release of nitric oxide from the vasc ular endothelium, thus prolonging the vasodilatation obtained using ea ch technique.