Prostanoids regulate proliferation of vascular smooth muscle cells inducedby arginine vasopressin

The aim of the present study was to investigate the effect of arginine [Arg (8)]vasopressin (vasopressin) on proliferation of vascular smooth muscle ce lls and the mechanisms underlying the action of vasopressin. To clarify the se issues, we used two different types of vascular smooth muscle cells, cul tured adult rat aortic smooth muscle cells and A10 cells, a cell line deriv ed from fetal rat aorta. Vasopressin (10(-8) to 10(-6) M) significantly sti mulated the proliferation of rat aortic smooth muscle cells in a dose-depen dent manner. In contrast, vasopressin significantly inhibited the prolifera tion of A10 cells. This inhibition was abolished when A10 cells were treate d with indomethacin. Vasopressin stimulated the production of prostanoids s everal-fold in A10 cells but not in rat aortic smooth muscle cells. These e ffects were completely blocked by the vasopressin V-1 receptor antagonist, 1-{1-[4-(3-acetylamino-propoxy)benzoyl]4-piperidyl)-3,4-dihydro-2(1H)-quino linone (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 vasopress in has diverse effect on proliferation of vascular smooth muscle cells thro ugh the vasopressin V-1 receptor, depending on the production of growth reg ulatory prostanoids. (C) 2000 Elsevier Science B.V. All rights reserved.