Participation of vascular prostacyclin for the pathogenesis of experimental glucocorticoid hypertension in rats.
Prostacyclin (PGI2) generation in the mesenteric arteries from dexamethasone acetate (DX) and deoxycorticosterone acetate (DOCA) treated rats was assessed by ex vivo perfusion method. PGI2 generation which was measured by 6-keto-PGF1 alpha output in the perfusate was significantly reduced in DX treated rats at prehypertensive stage both under the basal conditions and in response to angiotensin (ANG) II, whereas in DOCA group rats, vascular PGI2 production was not impaired. Plasma renin activity (PRA) was significantly suppressed in DOCA but normal in DX rats. These results suggest that the reduced PGI2 generation in the resistance arteries may contribute to the development of hypertension induced by DX.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure; D001835:Body Weight; D003900:Desoxycorticosterone; D003907:Dexamethasone; D011464:Epoprostenol; D006973:Hypertension / Q000139:chemically induced / Q000209:etiology*; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012083:Renin / Q000097:blood
D000804:Angiotensin II; D003900:Desoxycorticosterone; D003907:Dexamethasone; D011464:Epoprostenol; D012083:Renin; D009638:Norepinephrine