Blood pressure changes in spontaneously hypertensive rats correlate with aortic prostacyclin formation.
1 The relationship between the blood pressure fall, induced by antihypertensive drugs or bleeding, and the formation of prostacyclin (PGI2)-like activity in the thoracic aorta of spontaneously hypertensive rats has been investigated. Inhibition of ADP-induced platelet aggregation was used to assess PGI2-like activity. 2 The decreases in blood pressure produced by clonidine, dihydralazine and prazosin were associated with increases of PGI2-like activity of 50-80%. The increase in PGI2-like activity correlated well with the blood pressure decrease, independently of the mechanism of the fall in blood pressure.
D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001013:Aorta, Thoracic / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D003000:Clonidine / Q000494:pharmacology; D004078:Dihydralazine / Q000494:pharmacology; D011464:Epoprostenol / Q000096:biosynthesis* / Q000031:analogs & derivatives; D006973:Hypertension / Q000503:physiopathology*; D008297:Male; D011224:Prazosin / Q000494:pharmacology; D011453:Prostaglandins / Q000096:biosynthesis*; D051381:Rats
D000959:Antihypertensive Agents; D011453:Prostaglandins; C034240:prostaglandin I3; D011464:Epoprostenol; D003000:Clonidine; D004078:Dihydralazine; D011224:Prazosin