Endothelium-released adenosine triphosphate contributes to vasoconstrictor responses to periarterial nerve stimulation in isolated, perfused canine splenic arteries.

P2X-Purinoceptors and alpha1-adrenoceptors have previously been shown to be involved in double-peaked vasoconstrictor responses to periarterial electrical nerve stimulation in the isolated and perfused canine splenic artery. The present study was designed to investigate the influence of endothelium removal on vasoconstrictor responses to periarterial nerve stimulation, tyramine, noradrenaline, and adenosine triphosphate (ATP) in the isolated canine splenic artery. Intraluminal administration of saponin completely abolished the acetylcholine-induced vasodilatation and potentiated the vasoconstrictor response to KCl. Double-peaked vasoconstriction (two phases of vasoconstriction) was readily induced by periarterial electrical nerve stimulation in the canine splenic arterial preparation with or without endothelium and was consistently abolished by treatment with tetrodotoxin. Removal of endothelium slightly but significantly decreased the first-phase vasoconstrictor responses to stimulation of 1 or 10 Hz, and did not affect the second-phase. The vasoconstrictor responses to tyramine, noradrenaline, and ATP were not modified by endothelium removal. From these results, it is postulated that ATP released from endothelium, as a modulator of sympathetic nerve cotransmission, may partially contribute to the purinergic constriction component in the canine splenic artery.