M. Revington et al., SYMPATHETIC AND PARASYMPATHETIC INTERACTION IN VASCULAR AND SECRETORYCONTROL OF THE NASAL MUCOSE IN ANESTHETIZED DOGS, Journal of physiology, 505(3), 1997, pp. 823-831
1. In dogs anaesthetized with pentobarbitone, electrical stimulation o
f the parasympathetic nerve fibres to the nasal mucosa evoked frequenc
y dependent increases in both nasal arterial blood flow and nasal secr
etion. Blood flow was measured using a transonic flow probe placed aro
und the artery. 2. Sympathetic nerve stimulation for 3 min at 10 Hz ev
oked significant and prolonged (> 30 min) attenuation of the vasodilat
or and secretory responses to subsequent parasympathetic stimulation.
3. Intravenous and intranasal administration of the neuropeptide Y (NP
Y) analogue N-acetyl [Leu(28),Leu(31)] NPY 24-36, a selective NPY Y-2
receptor agonist (20 nmol kg(-1)), significantly attenuated both vasod
ilator and secretory effects of subsequent parasympathetic nerve stimu
lation. When given intravenously the inhibitory effect of this Y-2 rec
eptor agonist on vascular and secretory effects of parasympathetic ner
ve stimulation was rapid in onset (5 min) and lasted for more than 60
min. The modulatory effect of the Y-2 receptor agonist was also seen w
ith intranasal administration, but was slower in onset (15 min), and l
asted less than 45 min. The effects of the intranasal pretreatment wit
h the Y-2 receptor agonist were significantly prolonged in the presenc
e of the endopeptidase inhibitor phosphoramidon (10 nM). 4. Atropine p
retreatment did not significantly reduce the change in vascular conduc
tance evoked by parasympathetic nerve stimulation. Subsequent pretreat
ment with the NPY Y-2 receptor agonist N-acetyl [Leu(28),Leu(31)] NPY
24-36 reduced the stimulation induced increase in conductance by 30%.
Nasal secretion was reduced by 70% following pretreatment with atropin
e and a further 30% by pretreatment with the NPY Y-2 receptor agonist.
Dose dependent vasodilator and secretory effects of local intra-arter
ial infusion of acetylcholine and vasoactive intestinal peptide were n
ot modified by the NPY Y-2 agonist. 5. Total protein and albumin conce
ntration were measured in nasal lavage fluid collected after nerve sti
mulation. Atropine pretreatment increased the percentage of tile total
protein that was albumin in nasal lavage fluid. Neither sympathetic n
erve stimulation nor Y-2 receptor agonist pretreatment further modifie
d the albumin exudation (a marker of vascular permeability) in nasal f
luid las age collected after parasympathetic nerve stimulation. 6. We
propose that sympathetic nerve stimulation releases NPY, which acts on
Y-2 receptors, probably located on parasympathetic nerve endings, to
attenuate both vasodilatation and nasal secretion evoked by subsequent
parasympathetic nerve stimulation. This effect is also observed after
pretreatment with the Y-2-selective NPY analogue N-acetyl [Leu(28),Le
u(31)] NPY 24-36.