Heart rate decrease after inhibition of nitric oxide release in the anaesthetized dog.

In 5 anaesthetized vagotomized dogs the administration of an inhibitor of the synthesis of nitric oxide (NO) was seen to reduce the heart rate, although the arterial pressure was prevented from increasing. Such a finding suggests that the inhibition of nitric oxide release can produce bradycardia without the involvement of baroreceptor reflexes. Since NO inhibition is known to increase the concentration of adenosine in the myocardium, in 3 additional dogs, dipyridamole, which also potentiates the effect of adenosine, was infused: a reduction in heart rate was observed also in these animals. In both groups of animals, before and after the administration of the relevant compound, the increase in ABP obtained with aortic constriction caused the same reduction in heart rate, which which was attributed to a reduction of the basal sympathetic discharge, which was shown not to be affected by NO inhibition. It is concluded that NO inhibition can cause bradycardia without the intervention of any nervous mechanism but with the possible intervention of an increase in myocardial adenosine concentration.