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Prejunctional prostanoid receptors on cardiac adrenergic terminals belong to the EP 3 subtype
Author(s) -
Mantelli Laura,
Amerini Sandra,
Rubino Annalisa,
Ledda Fabrizio
Publication year - 1991
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.1476-5381.1991.tb12214.x
Subject(s) - stimulation , medicine , endocrinology , adrenergic , antagonist , contractility , prostanoid , chemistry , receptor , prostaglandin e , inhibitory postsynaptic potential , prostaglandin
1 The effects of prostaglandin E 2 (PGE 2 ) and of several synthetic prostanoids on the cardiac response to sympathetic nerve stimulation in guinea‐pig atria have been evaluated. 2 PGE 2 (0.01–100 n m ), sulprostone (0.01–100 n m ) and misoprostol (0.1–100 n m ), but not butaprost (0.1–100 n m ), dose‐dependently reduced the increase in cardiac contractility induced by electrical field stimulation of sympathetic terminals. 3 The EP 1 antagonist AH6809 (1 μ m ) did not modify the inhibition of cardiac response induced by PGE 2 , sulprostone and misoprostol. 4 In preparations preloaded with [ 3 H]‐noradrenaline, tritium overflow induced by electrical field stimulation was greatly and significantly reduced by 100 n m PGE 2 and by 100 n m sulprostone. 5 These results indicate that PGE 2 and other synthetic prostanoids reduce noradrenaline release from cardiac adrenergic nerve terminals acting on prejunctional inhibitory receptors belonging to the EP 3 subtype.