title: Prostanoids regulate proliferation of vascular smooth muscle cells induced by arginine vasopressin.
abstract: The aim of the present study was to investigate the effect of arginine [Arg(8)]vasopressin (vasopressin) on proliferation of vascular smooth muscle cells and the mechanisms underlying the action of vasopressin. To clarify these issues, we used two different types of vascular smooth muscle cells, cultured adult rat aortic smooth muscle cells and A10 cells, a cell line derived from fetal rat aorta. Vasopressin (10(-8) to 10(-6) M) significantly stimulated the proliferation of rat aortic smooth muscle cells in a dose-dependent manner. In contrast, vasopressin significantly inhibited the proliferation of A10 cells. This inhibition was abolished when A10 cells were treated with indomethacin. Vasopressin stimulated the production of prostanoids several-fold in A10 cells but not in rat aortic smooth muscle cells. These effects were completely blocked by the vasopressin V(1) receptor antagonist, 1-¿1-[4-(3-acetylamino-propoxy)benzoyl]4-piperidyl¿-3, 4-dihydro-2(1H)-quinolinone (OPC21268), but not by the vasopressin V(2) receptor antagonist, (+/-)-5-dimethylamino-1-[4-(2-methylbenzoylamino)benzol]-2, 3,4,5-tetrahydro-1H-benzazepine hydrochloride (OPC31260). These results indicate that vasopressin has diverse effect on proliferation of vascular smooth muscle cells through the vasopressin V(1) receptor, depending on the production of growth regulatory prostanoids.
authors.affiliation: Department of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Nagano
authors.forename: K
authors.initials: K
authors.lastname: Toba
authors.forename: M
authors.initials: M
authors.lastname: Akishita
authors.forename: T
authors.initials: T
authors.lastname: Watanabe
authors.forename: K
authors.initials: K
authors.lastname: Kozaki
authors.forename: M
authors.initials: M
authors.lastname: Eto
authors.forename: M
authors.initials: M
authors.lastname: Hashimoto
authors.forename: N
authors.initials: N
authors.lastname: Sudoh
authors.forename: J
authors.initials: J
authors.lastname: Ako
authors.forename: M
authors.initials: M
authors.lastname: Yoshizumi
authors.forename: Y
authors.initials: Y
authors.lastname: Ouchi
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis / Q000502:physiology; D000818:Animals; D001013:Aorta, Thoracic; D001127:Arginine Vasopressin / Q000494:pharmacology*; D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D002478:Cells, Cultured; D004247:DNA / Q000096:biosynthesis; D015232:Dinoprostone / Q000096:biosynthesis / Q000502:physiology; D004305:Dose-Response Relationship, Drug; D004622:Embryo, Mammalian; D011464:Epoprostenol / Q000096:biosynthesis / Q000502:physiology; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000166:cytology* / Q000187:drug effects* / Q000378:metabolism; D011453:Prostaglandins / Q000096:biosynthesis / Q000502:physiology*; D051381:Rats; D013929:Thromboxane B2 / Q000096:biosynthesis / Q000502:physiology
chemical_list: D011453:Prostaglandins; D001127:Arginine Vasopressin; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D004247:DNA; D011464:Epoprostenol; D015232:Dinoprostone