Article date: October 1994
By: J. Silvain Lacroix, Lesley G. Ulman, Erica K. Potter, in Volume 113, Issue 2, pages 479-484
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, 1ms, 10–30 Hz) evoked frequency‐dependent vasodilatation.
Sympathetic nerve stimulation for 3min 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.
Vasodilator effects of exogenous vasoactive intestinal polypeptide and peptide histidine isoleucine and vasoconstrictor effects of exogenous neuropeptide Y (NPY) and the NPY analogue [Leu31, Pro34] NPY (Y1‐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 [Leu28, Leu31] NPY 24–36 (Y2‐receptor agonist, 20 nmol kg−1) but not by exogenous Y1receptor agonist. The Y2‐receptor agonist did not show significant vasoconstrictor action.
It is concluded that sympathetic nerve stimulation attenuates parasympathetic vasodilatation via NPY release acting on prejunctional Y2 receptors.
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, 1ms, 10–30 Hz) evoked frequency‐dependent vasodilatation.
Sympathetic nerve stimulation for 3min 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.
Vasodilator effects of exogenous vasoactive intestinal polypeptide and peptide histidine isoleucine and vasoconstrictor effects of exogenous neuropeptide Y (NPY) and the NPY analogue [Leu31, Pro34] NPY (Y1‐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 [Leu28, Leu31] NPY 24–36 (Y2‐receptor agonist, 20 nmol kg−1) but not by exogenous Y1receptor agonist. The Y2‐receptor agonist did not show significant vasoconstrictor action.
It is concluded that sympathetic nerve stimulation attenuates parasympathetic vasodilatation via NPY release acting on prejunctional Y2 receptors.
DOI: 10.1111/j.1476-5381.1994.tb17014.x
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