The Vasodilator Properties of Noradrenaline in the Human Forearm

The stimulant effects of noradrenaline on the heart are readily blocked by sympathetic /3-receptor antagonists (Moran & Perkins, 1958; McInerny, Gilmour & Blinks, 1965; Brick, Hutchison & Roddie, 1966a).This indicates that noradrenaline can stimulate P-receptors.The powerful vasodilator effect of isoprenaline in the human forearm is also blocked by /3-receptor antagonists (Glover, Greenfield & Shanks, 1962).This indicates that P-receptors occur in the smooth muscle in forearm blood vessels.It is, therefore, to be expected that noradrenaline would have some vasodilator properties in the forearm.Glover & Hutchison (1965) found evidence that this is the case.They showed that the ,8-receptor antagonist, propranolol, increased the vasoconstrictor response in the human forearm to intravenous infusions of noradrenaline.When given intra-arterially in the forearm, noradrenaline causes intense vasoconstric- tion, so it is clear that any vasodilatation due to stimulation of /3-receptors is normally masked by the more powerful stimulation of a-receptors.However, if the vasoconstrictor effects of noradrenaline were blocked with an a-receptor antagonist, noradrenaline would be expected to cause vasodilatation in the forearm.It is, therefore, surprising that Allwood & Ginsburg (1961) found that the vasoconstrictor response to noradrenaline in the forearm was not reversed after pharmacological blockade of a-receptors with phenoxy- benzamine.This inconsistency led to the present experiments, which show that the vasoconstrictor response to noradrenaline is readily reversed if suitable doses of nor- adrenaline and a-receptor antagonist are used.Phentolamine was used to block a-receptors since its high solubility and relatively short-lived action permitted high con- centrations of the drug to be used.A preliminary account of some of these findings has already been published (Brick, Hutchison & Roddie, 1966b).