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Vasoconstriction of guinea‐pig submucosal arterioles following sympathetic nerve stimulation is mediated by the release of ATP
Author(s) -
Evans R.J.,
Surprenant A.
Publication year - 1992
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1992.tb14323.x
Subject(s) - excitatory postsynaptic potential , vasoconstriction , postsynaptic potential , stimulation , medicine , prazosin , endocrinology , rauwolscine , chemistry , inhibitory postsynaptic potential , biology , antagonist , receptor
1 The nature of the transmitter mediating vasoconstriction of guinea‐pig submucosal arterioles following sympathetic nerve stimulation was studied. 2 Prazosin (0.1 μ m ) abolished the response to exogenously applied phenylephrine (1 μ m ) but had no effect on constrictions of submucosal arterioles evoked by nerve stimulation (100 pulses at 10 Hz). 3 Vasoconstrictions and excitatory junction potentials elicited by nerve stimulation were potentiated by idazoxan (0.1 μ m ). 4 Following reserpine treatment, catecholamine fluorescence was absent in submucosal arterioles but nerve‐evoked vasoconstrictions were unaltered. 5 Vasoconstrictions and excitatory junction potentials recorded in response to sympathetic nerve stimulation, as well as constrictions evoked by exogenously applied ATP (3 μ m ), were abolished by the P 2 ‐purinoceptor antagonist, suramin (100 μ m ). Suramin had no effect on the vasoconstriction in response to noradrenaline (3 μ m ), or the nicotinic excitatory postsynaptic potentials (e.p.s.ps) and noradrenergic inhibitory postsynaptic potentials (i.p.s.ps) recorded from submucosal neurones. 6 We conclude that postjunctional responses of submucosal arterioles following sympathetic nerve stimulation are mediated solely through the activation of P 2X ‐purinoceptors by ATP or a related purine nucelotide. The function of neurally released noradrenaline is to act through prejunctional α 2 ‐adrenoceptors to depress transmitter release.