MODULATION BY NEUROPEPTIDE-Y OF PARASYMPATHETIC NERVE-EVOKED NASAL VASODILATATION VIA Y-2 PREJUNCTIONAL RECEPTOR

1 In pentobarbitone anaesthetized dogs, preganglionic stimulation of the superior cervical sympathetic nerve (15 V, 1 ms, 10 Hz) induced marked reduction of nasal arterial blood flow, whereas parasympathetic nerve stimulation (5 V, 1 ms, 10-30 Hz) evoked frequency-dependent vasodilatation. 2 Sympathetic nerve stimulation for 3 min at 10 Hz evoked significant (P<0.05) and prolonged attenuation of the vasodilator response to subsequent parasympathetic stimulation. Pretreatment with phentolamine (0.5 mg kg(-1) h(-1)), propranolol (1 mg kg(-1)) and atropine (0.5 mg kg(-1)) reduced the vasoconstrictor effect of sympathetic stimulation by 35 +/- 4% whereas the parasympathetic nerve-evoked vasodilatation was not significantly modified. Atropine-resistant parasympathetic vasodilatation remained significantly attenuated for more than 30 min after non-adrenergic sympathetic nerve-evoked vasoconstriction. 3 Vasodilator effects of exogenous vasoactive intestinal polypeptide and peptide histidine isoleucine and vasoconstrictor effects of exogenous neuropeptide Y (NPY) and the NPY analogue [Leu(31), Pro(34)] NPY (Y-1-receptor agonist, 8 nmol kg(-1)), were not altered by adrenoceptor antagonists and atropine whereas the effects of exogenous noradrenaline and acetylcholine were virtually abolished. Attenuation of parasympathetic-evoked vasodilatation could be mimicked by exogenous NPY (8 nmol kg(-1)) and the NPY analogue, N-acetyl [Leu(28), Leu(31)] NPY 24-36 (Y-2-receptor agonist, 20 nmol kg(-1)) but not by exogenous Y-1-receptor agonist. The Y-2-receptor agonist did not show significant vasoconstrictor action. 4 It is concluded that sympathetic nerve stimulation attenuates parasympathetic vasodilatation via NPY release acting on prejunctional Y-2 receptors.