Dissociation of potentiation of Leu31 Pro34 neuropeptide Y on adrenergic and purinergic transmission in isolated canine splenic artery.

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 alpha1-adrenoceptors or Y1 receptors with 0.1 microM prazosin or with 1 microM BIBP 3226 ((R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-argininami de), respectively. The remaining responses in the presence of LP-NPY and prazosin were abolished by P2X receptor desensitization with 1 microM alpha,beta-methylene ATP. Moreover, 30 nM LP-NPY failed to modify the vasoconstrictor responses to nerve stimulation after treatment with prazosin. A subsequent administration of alpha,beta-methylene ATP completely suppressed the remaining responses after prazosin and LP-NPY. The vasoconstrictions induced by 0.003-1 nmol noradrenaline and 0.003-1 micromol 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.