Abstract
Double-peaked vasoconstrictor responses to periarterial nerve electrical stimulation (PNS) were readily induced in the condition of 30-s trains of pulses in isolated, perfused canine splenic artery, using the cannula insertion technique. P2X purinoceptors have been shown to be involved mainly in the 1st peaked response and α1 adrenoceptors mostly in the 2nd one. Administrated NPY induced no direct vasoconstriction or only a slight vasoconstriction, and it inhibited the double-peaked vasoconstriction in a dose-related manner. A small dose of NPY Y1-receptor agonist, L-P NPY, readily potentiated the 2nd peaked response to PNS, and an increasing dose of LP-NPY did both the 1st and 2nd peaked responses. The 2nd peaked response was significantly inhibited by treatment with chloroethylclonidine (CEC), an α1B-adrenoceptor antagonist, but the 1st peaked response was not influenced. On the other hand, an α1A-antagonist, WB4101, rather potentiated the 2nd peaked response, although it did not modify the 1st one. Administered NA-induced constrictions were consistently inhibited by WB4101 but not by CEC. From these results, it is concluded that NPY inhibits the release of ATP and NA from periarterial nerve terminals by activation of presynaptic NPY Y2 receptors, and it potentiates PNS-induced vasoconstrictions via α1B-adrenoceptors by activation of postjunctional NPY Y1 receptors in the canine splenic artery.
