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1 Department of Physiology and 2 Department of Pharmacology and Therapeutics, School of Medicine, Queen's University Belfast, Medical Biology Centre, Belfast, BT9 7BL United Kingdom
We examined the contributions of
the cotransmitters norepinephrine (NE), ATP, and neuropeptide Y (NPY)
to sympathetically evoked vasoconstriction in the rat tail artery in
isolated vascular rings by using 1-100 stimulation impulses at 20 Hz. Phentolamine (2 µM), the 
-adrenoceptor antagonist, markedly
reduced responses to all stimuli, although responses to lower impulse
numbers were reduced less than responses to longer trains. The
purinergic receptor antagonist suramin (100 µM) reduced all
responses, but to a much greater extent with few impulse trains.
Responses were further reduced or abolished by addition of the second
antagonist. Any remaining responses were abolished by the
NPY-Y1 receptor antagonist BIBP-3226 (75 nM). NPY had a
direct agonist action and potentiated sympathetically mediated
responses. NPY (75 nM) potentiated responses and BIBP-3226 decreased
responses to 2- and 20-impulse trains. Both affected responses from 2 impulses to >20 impulses, but there was no preferential effect on
purinergic contributions to responses because neurally released NPY
potentiated both "pure" NE and ATP responses equally. We conclude
that all three cotransmitters contribute significantly to vascular
responses and their contribution varies markedly with impulse numbers.
There is considerable synergy between cotransmitters, especially with
lower impulse numbers where NPY contributions are greater than expected.
norepinephrine; ATP; neuropeptide Y; impulse patterning; synergy
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