Participation of vascular prostacyclin for the pathogenesis of experimental glucocorticoid hypertension in rats

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 trea...

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Bibliographic Details
Published in:Clinical and experimental hypertension. Part A, Theory and practice Vol. 7; no. 4; p. 513
Main Authors: Miyamori, I, Yasuhara, S, Ikeda, M, Koshida, H, Takeda, Y, Morise, T, Nagai, K, Okamoto, S, Takeda, R
Format: Journal Article
Language:English
Published: United States 1985
Subjects:
Angiotensin II - pharmacology
Animals
Blood Pressure
Body Weight
Desoxycorticosterone
Dexamethasone
Epoprostenol
Hypertension - chemically induced
Hypertension - etiology
Male
Norepinephrine - pharmacology
Rats
Rats, Inbred Strains
Renin - blood
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Summary: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.
ISSN:0730-0077
DOI:10.3109/10641968509077209