Prostacyclin effects on the blood pressure responses to norepinephrine in rats treated with aspirin or indomethacin.
The atherosclerotic condition is associated with a reduction of PGI2 synthesis; moreover, in the presence of elevated serum cholesterol levels, pressor responses to norepinephrine are potentiated. In order to verify if a complete inhibition of PGI2 production affects the vascular reactivity, it was assayed two cycloxygenase inhibitors (lysine acetylsalicylate and indomethacin) in rats. The two drugs significantly potentiated the blood pressure responses to norepinephrine, and completely inhibited PGI2-like substances production by arterial rings. The prostacyclin infusion (15 ng/kg/min, i.v.) completely reversed such potentiation, without any major modification in the basal blood pressure values. These results show that PGI2 production is responsible for vascular tone modulation and may partially explain the altered vascular reactivity in the atherosclerotic condition.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D001794:Blood Pressure / Q000187:drug effects*; D011464:Epoprostenol / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects; D009638:Norepinephrine / Q000494:pharmacology*; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats
D011453:Prostaglandins; D011458:Prostaglandins E; D011464:Epoprostenol; D001241:Aspirin; D009638:Norepinephrine; D007213:Indomethacin