Abstract

A sustained vasodilatation occurs in the perfused dog hindlimb during lumbar sympathetic chain stimulation after inactivation or depletion of adrenergic neurons. The existence of the vasodilator system is more easily demonstrated after administration of drugs which deplete or prevent release of adrenergic amines, suggesting that the sustained dilator system is largely masked, or prevented from being activated, by the functionally discharging adrenergic system. The purpose of the present investigation was to explore the possibility that sustained dilatation occurs as a result of change in the function of adrenergic neurons from vasoconstriction to vasodilatation. It is concluded that sustained dilatation does not result from neurosecretion of adrenergic antirelease or depleting agents because stimulation of the lumbar sympathetic nerves in dogs pretreated with reserpine results in large sustained dilatations even though reserpine, itself, fails to elicit a vascular dilatation in pretreated dogs. Xylocholine and guanethidine are capable of producing large vascular dilatations in the dog depleted of adrenergic amines, but the dose required to produce dilatation exceeds by more than 10.000 times the theoretical amount which would be released from nerve endings if these agents functioned as false transmitters. Intermediates of adrenergic amine synthesis and adrenergic metabolites have also been ruled out as potential false transmitters of adrenergic neurons. Evidence has also been obtained that the sustained dilator system can be activated in the absence of drug treatment. This latent sympathetic vasodilator system is therefore deemed to be physiologically and anatomically separate from the adrenergic system.