Prostacyclin (PGI2) synthesis in the vascular wall of rats with bilateral renal artery stenosis.
The ability of vessels (rings of arteries and vena cava) to synthesize prostacyclin (PGI2) "in vitro" was analyzed in the initial (6-day) and chronic (6-week) phase of two-kidney, two clip hypertension. Male Wistar CHbb THOM rats were used. Tissues were incubated for two hours in Krebs solution containing 14C-arachidonic acid as exogenous substrate. Specimens (in benzene-ethanol 4:1 vol/vol) and the unlabeled standard solutions of arachidonic acid, 6-keto PGF1 alpha, PGF2 alpha, and PGE2, were spotted on silica gel-G plates for thin layer chromatography. Conversion of 14C-arachidonic acid to stable metabolite 6-keto PGF1 alpha was used as an index of PGI2 synthesis. Results shown: 1) PGI2 is the major PG synthesized by the rat artery wall; 2) PGI2 synthesis was increased 2.4 times in the initial 6-day period of development of renovascular hypertension (RH); 3) no changes in PGI2 production were observed in arteries during the chronic 6-week period of RH; 4) abdominal vena cava has little or no capacity to produce PGI2. As PGI2 is a potent vasodilator, higher production by arteries during the 6-day period suggests that prostacyclin could play a modulator role on peripheral resistance during the initial phase of renal hypertension.
D000818:Animals; D001158:Arteries / Q000378:metabolism; D001808:Blood Vessels / Q000378:metabolism*; D011464:Epoprostenol / Q000096:biosynthesis*; D006978:Hypertension, Renovascular / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012078:Renal Artery Obstruction / Q000378:metabolism*; D014655:Vascular Resistance; D014680:Veins / Q000378:metabolism
D011464:Epoprostenol