CHARACTERIZATION OF THE NEUROGENIC VASODILATATION ELICITED BY CENTRAL DOPAMINE RECEPTOR STIMULATION WITH PERGOLIDE

  • 1 January 1984
    • journal article
    • research article
    • Vol. 228  (3) , 696-703
Abstract
Bilateral hindlimb perfusion at controlled flow rates was used to investigate centrally mediated actions of the dopamine receptor agonist pergolide on hindlimb vascular resistance in anesthetized dogs. Intracisternal administration of pergolide caused sustained hypotension, bradycardia and a decrease in perfusion pressure in the innervated hindlimb, whereas prefusion pressure in the denervated limb was not altered by pergolide. The pressure-flow curves were shifted to the right in the innervated hindlimb but not in the denervated limb, suggesting that pergolide caused neurogenic dilatation in the hindlimb vasculature. I.v. administration of the same dose of pergolide elicited transient hypertension and marked vasoconstriction in the denervated limb. Hypotension and neurogenic hindlimb vasodilatation of lesser magnitude than that produced by intracisternal pergolide were seen only 40-50 min after administration of i.v. pergolide. The hindlimb vasodilator action of intracisternal pergolide could be antagonized by sulpiride, which suggests that activation of central dopamine receptors was responsible for the action of pergolide. Because the neural innervation to the hindlimb is comprised of sympathetic vasoconstrictor as well as cholinergic and dopaminergic vasodilator fibers, additional experiments were performed to determine the mechanisms inovolved in the neurogenic vasodilatation caused by pergolide. Treatment with atropine did not alter the neurogenic decrease in the hindlimb vascular resistance produced by pergolide, indicating that activation of cholinergic vasodilator fibers was not responsible for this phenomenon. Phentolamine treatment completely abolished the hindlimb vasodilatation seen with pergolide, which rules out the involvement of dopaminergic fibers in the action of pergolide. Central dopamine receptor stimulation evidently produces a neurogenic dilatation in the hindlimb vasculature which is due to the inhibition of sympathetic vasoconstrictor tone to the hindlimb and does not involve activation of either cholinergic or dopaminergic vasodilator fibers.