title: Catecholamines are not linked to myometrial phospholipase C and uterine contraction in late pregnant and parturient mouse.
abstract: 1. We investigated whether catecholamines through activation of alpha(1)-adrenergic receptors (alpha(1)-AR) are involved in mouse uterine contraction at parturition. Myometrial phospholipase C (PLC) activity and uterine contraction were measured in response to noradrenaline (NA), the specific alpha(1)-AR agonist phenylephrine (Phe) and oxytocin (OT). 2. Using the reverse transcription-polymerase chain reaction RT-PCR, we detected the alpha(1a)-AR subtype in late pregnant mouse myometrium. We also detected, by immunoblotting studies, PLCbeta(1), PLCbeta(3) and different alpha-subunits of pertussis toxin-insensitive (Galpha(q/11)) and -sensitive G proteins (Galpha(o/i3), Galpha(i1/2)). 3. Phenylephrine and NA did not alter the myometrial inositol phosphate (InsP) production of late pregnant or parturient mouse. In similar conditions, OT increased InsP production in a dose-dependent manner. Consistent with these results, only OT (10 microM) recruited PLCbeta(1) and PLCbeta(3) to myometrial plasma membranes. The OT-induced InsP response was not altered by pertussis toxin (300 ng ml(-1), 2 h pretreatment), suggesting the involvement of a member of the Galpha(q) family. 4. Noradrenaline and Phe failed to increase uterine contraction at late pregnancy and at parturition. In contrast, OT induced uterine contraction in a dose-dependent manner with maximal increase (400 %) at a concentration of 1 microM. 5. The results indicate that OT receptors (OTR) but not alpha(1)-AR are linked to myometrial PLC activation and uterine contraction in late pregnant and parturient mouse. This discrepancy between mouse and other mammals could be attributed to the alpha(1)-AR subtype expressed in myometrium at this time.
authors.affiliation: Laboratoire de Physiologie de la Reproduction, CNRS ESA 7080, Université Pierre et Marie Curie, 75252 Paris Cedex 05, France. Sakina.Mhaouty-Kodja@snv.jussieu.fr
authors.forename: S
authors.initials: S
authors.lastname: Mhaouty-Kodja
authors.forename: E
authors.initials: E
authors.lastname: Houdeau
authors.forename: J
authors.initials: J
authors.lastname: Cohen-Tannoudji
authors.forename: C
authors.initials: C
authors.lastname: Legrand
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D002462:Cell Membrane / Q000201:enzymology; D005260:Female; D015870:Gene Expression / Q000502:physiology; D007295:Inositol Phosphates / Q000096:biosynthesis; D007527:Isoenzymes / Q000032:analysis / Q000378:metabolism*; D007743:Labor, Obstetric / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D009215:Myometrium / Q000201:enzymology*; D009638:Norepinephrine / Q000494:pharmacology*; D010121:Oxytocin / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D054799:Phospholipase C beta; D011247:Pregnancy; D011433:Propranolol / Q000494:pharmacology; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D018340:Receptors, Adrenergic, alpha-1 / Q000235:genetics / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction / Q000502:physiology; D013566:Sympathomimetics / Q000494:pharmacology*; D010738:Type C Phospholipases / Q000032:analysis / Q000378:metabolism*; D014590:Uterine Contraction / Q000187:drug effects / Q000502:physiology*
chemical_list: D000319:Adrenergic beta-Antagonists; D007295:Inositol Phosphates; D007527:Isoenzymes; D012333:RNA, Messenger; D018340:Receptors, Adrenergic, alpha-1; D013566:Sympathomimetics; D010656:Phenylephrine; D010121:Oxytocin; D011433:Propranolol; D010738:Type C Phospholipases; D054799:Phospholipase C beta; D009638:Norepinephrine