Abstract
1 In the rabbit portal veins, cocaine potentiated responses to (-)-noradrenaline, and prolonged relaxation following transmural stimulation. Neither process was altered by hydrocortisone and U-0521, oxytetracycline or 4-aminopyridine alone or in combination with cocaine. These findings indicated that neuronal uptake was principally responsible for the inactivation of noradrenaline in this tissue. 2 In the rabbit pulmonary artery, the rate of relaxation following transmural stimulation was prolonged by cocaine and by hydrocortisone and U-0521, and further prolonged by the combination of all three drugs. These findings suggest that both neuronal and extra-neuronal uptake are responsible for the inactivation of noradrenaline in this tissue. 3 4-Aminopyridine potentiated responses to (-)-noradrenaline and prolonged relaxation after transmural stimulation in pulmonary artery possibly as a consequence of a postjunctional action in this tissue. 4 The rabbit portal vein was less sensitive to (-)-noradrenaline and relaxed more after transmural stimulation than the pulmonary artery. It is suggested that this reflects the denser noradrenergic innervation and smaller neuromuscular distance present in the portal vein.