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Elevation of plasma noradrenaline levels in urethane‐anaesthetized rats by activation of central prostanoid EP 3 receptors
Author(s) -
Yokotani Kunihiko,
Nishihara Makoto,
Murakami Yoshinori,
Hasegawa Takashi,
Okuma Yasunobu,
Osumi Yoshitsugu
Publication year - 1995
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.1476-5381.1995.tb14985.x
Subject(s) - agonist , endocrinology , medicine , prostanoid , chemistry , receptor , prostaglandin e2 receptor , antagonist , prostaglandin , potency , pharmacology , biology , in vitro , biochemistry
1 We studied the effects of intracerebroventricular (i.c.v.) administration of prostaglandin E 2 (PGE2) and its receptor subtype ligands on plasma levels of catecholamines in urethane‐anaesthetized rats. 2 Administration of PGE 2 (0.15, 0.3 and 1.5 nmol per animal, i.c.v.) dose‐dependently elevated plasma levels of noradrenaline (NA), while the levels of adrenaline were not affected. 3 Administration of sulprostone (EP 3 /EP 1 agonist) and misoprostol (EP 3 /EP 2 agonist) effectively elevated plasma NA levels in a dose‐dependent manner (0.1, 0.3, and 1.0 nmol per animal). Butaprost (EP 2 agonist) (0.3, 1.0 and 3.0 nmol per animal) was without effect. 17‐Phenyl‐ω‐trinor PGE 2 (EP 1 /EP 3 agonist) effectively elevated plasma NA levels only at its highest dose (1.0 nmol per animal), but this elevation was not attenuated by pretreatment with SC‐19220 (selective EP 1 antagonist) (20 nmol per animal, i.c.v.). 4 The potency of these test agents in elevating plasma levels of NA was as follows; misoprostol > sulprostone > PGE 2 > > 17‐phenyl‐ω‐trinor PGE 2 > > > butaprost. These results suggest that activation of central prostanoid EP 3 ‐receptors induces central sympathetic outflow in rats.