Participation of Vascular Prostacyclin for the Pathogenesis of Experimental Glucocorticoid Hypertension in Rats

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Abstract
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. [6-keto-prostaglandin F1.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; in DOCA group rats, vascular PGI2 production was not impaired. Plasma renin activity (PRA) was significantly suppressed in DOCA but normal in DX rats. The reduced PGI2 generation in the resistance arteries may evidently contribute to the development of hypertension induced by DX.