Purinergic and adrenergic cotransmission in @entity235 isolated and perfused XXXX .

@entity2997 @entity3160 @entity235 @entity3159 @entity1022 @entity4763 @entity861 @entity432 @entity1063 @entity5747 @entity855
1. The vasoconstrictor responses of @entity235 @entity432 to periarterial electrical nerve stimulation (PNS; 30 s trains of pulses at a frequency of 2, 4 or 8 Hz) were observed in a frequency dependent manner. The PNS-induced vasoconstrictions were abolished by @entity1022 (1 micromol/L) and mostly depressed but not completely by @entity2997 (10 micromol/L). 2. Vasoconstrictor responses to administered @entity1063 were antagonized significantly by @entity3159 (0.1 micromol/L), an alpha1-adrenoceptor antagonist, but were not significantly affected by @entity5747 (100 micromol/L), a P2 purinoceptor antagonist, or @entity861 (1 micromol/L), a P2X receptor desensitizing agent. Exogenous @entity855 -induced responses were clearly depressed by @entity5747 or @entity861 , but were not significantly affected by @entity3159 . 3. The vasoconstrictor responses to PNS at a low frequency (2 and 4 Hz) of stimulation were markedly inhibited by @entity5747 (100 micromol/L) and by @entity861 (1 micromol/L). The remaining responses after @entity5747 or @entity861 were abolished by subsequent application of @entity3159 (0.1 micromol/L). At a high frequency (8 Hz) of stimulation, the vascular response was not significantly inhibited by @entity5747 or @entity861 , but it was abolished by @entity3159 . 4. Injection of @entity4763 (0.3-30 nmol/L), an alpha2-adrenoceptor agonist, did not induce any clear vasoconstriction. The exposure of tissues to @entity3160 (0.1-0.3 micromol/L), an alpha2-adrenoceptor antagonist, dose-dependently increased PNS-induced vasoconstrictions at all frequencies tested. 5. The present results indicate that @entity855 acts as a cotransmitter with @entity1063 and is responsible for post-junctional vasoconstrictor responses at low frequencies of sitmulation, whereas the effect of @entity1063 is dominant at high-frequency stimulation in @entity235 @entity432 . Prejunctional alpha2-adrenoceptor autoinhibition may modulate the release of either @entity1063 or @entity855 from sympathetic nerve terminals.
