Dissociation of Potentiation of Leu³¹ Pro³⁴ Neuropeptide Y on Adrenergic and Purinergic Transmission in Isolated Canine Splenic Artery

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The present study observed the effects of an activation of neuropeptide Y(NPY)Y₁ receptors on adrenergic and purinergic components of double−peaked vasoconstrictor responses to periarterial nerve stimulation in the isolated, perfused canine splenic arteries.The results showed that 3−30 nM Leu³¹ Pro³⁴ neuropeptide Y(LP−NPY)produced a dose−dependent potentiation of double−peaked vasoconstrictor responses to trains of 30−s pulses at 1, 4 or 10 Hz of stimulation.The potentiation of LP−NPY of the nerve−stimulated vasoconstrictions were completely inhibited by subsequent blockade of α₁−adrenoceptors or Y₁ receptors with 0.1μM prazosin or with 1μM BIBP 3226((R)−N²−(diphenylacetyl)−N−[(4−hydroxyphenyl)methyl]−argininamide), respectively.The remaining responses in the presence of LP−NPY and prazosin were abolished by P2X receptor desensitization with 1μM α, β−methylene ATP.Moreover, 30 nM LP−NPY failed to modify the vasoconstrictor responses to nerve stimulation after treatment with prazosin.A subsequent administration of α, β−methylene ATP completely suppressed the remaining responses after prazosin and LP−NPY.The vasoconstrictions induced by 0.003−1 nmol noradrenaline and 0.003−1μmol ATP were slightly, but not significantly enhanced by 30 nM LP−NPY.The observations indicated that activation of postjunctional NPY Y₁ receptors may have an important role in the modulation of adrenergic rather than purinergic transmission of the sympathetic co−transmission.