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Inhibitory 5‐hydroxytryptamine receptors involved in pressor effects obtained by stimulation of sympathetic outflow from spinal cord in pithed rats
Author(s) -
Morán A.,
Velasco C.,
Salvador T.,
Martín M.L.,
Román L. San
Publication year - 1994
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.1476-5381.1994.tb17147.x
Subject(s) - stimulation , inhibitory postsynaptic potential , spinal cord , receptor , endocrinology , medicine , outflow , sympathetic nervous system , serotonin , chemistry , neuroscience , biology , blood pressure , physics , meteorology
1 A study was made of the effects of 5‐hydroxytryptamine (5‐HT) on pressor response induced in vivo by electrical stimulation of the sympathetic outflow from the spinal cord of pithed rats. All animals had been pretreated with atropine. Intravenous infusion of 5‐hydroxytryptamine at doses of 10 and 20 μg kg −1 min −1 reduced the pressor effects obtained by electrical stimulation at intervals of 10 min over the 1 h of infusion. 2 This inhibitory action of 5‐HT was depressed by cyproheptadine and methiothepin but was not modified by ketanserin or MDL‐72222. By contrast, the inhibitory action of 5‐HT was lost in pithed rats that had been pretreated with exogenous noradrenaline. 3 The 5‐HT 1 receptor agonist 5‐carboxamidotryptamine (5‐CT) caused an inhibition of the pressor response, whereas the 5‐HT 3 receptor agonist, 1‐phenylbiguanide, produced a variable but significant increase in the pressor response. The 5‐HT 2 receptor agonist, m‐CPP, did not modify the pressor sympathetic response. 4 Our results suggest that 5‐hydroxytryptamine interferes with sympathetic neurotransmission by inhibiting pressor effects as a result of stimulation of the complete sympathetic outflow, and that this inhibition is mainly through a presynaptic 5‐HT 1 mechanism.