Further Evidence for 'Active' Reflex Vasodilatation

Abstract

Further experimental evidence has been presented which strengthens the hypothesis of active reflex dilatation. The administration of a ganglionic blocking agent in a dose sufficient to block completely adrenergic tone failed to lower the perfusion pressure in the isolated extremity to the same level as was reached during the nadir of reflex dilatation. Thus, it is reaffirmed that simple withdrawal of adrenergic vascular tone (passive reflex dilatation) cannot entirely account for the total magnitude of reflex dilatation. Although chronic reserpine pretreatment eliminated both reflex constriction and dilatation, acute reserpine administration reduced reflex dilatation at a time when reflex constriction and perfusion pressure were little affected. On the other hand, the administration of the substituted phenothiazine, methotrimeprazine, eliminated adrenergic tone but had little effect on reflex dilatation. The latter two types of experiment provide further important dissociations between reflex dilatation and inhibition of existing adrenergic activity. Administration of cocaine by several different routes reduced reflex dilatation, but the reduction in reflex dilatation does not appear to be due to inhibition of reuptake of adrenergic amine. Neither does blockade of active reflex dilatation by the antihistamine, tripelennamine, appear to be related to its possible ability to block reuptake of adrenergic amine. Classic autoregulatory stimuli fail to elicit a response analogous to active reflex vasodilatation, and antihistamines fail to alter autoregulatory readjustments while reducing very effectively active reflex vasodilatation.