Effects of nitroglycerin on human vascular prostacyclin and thromboxane A2 generation.
We examined the effects of NTG on human saphenous and umbilical vein PGI2 and TXA2 generation. Vascular rings from both types of vessels generated TXA2 in addition to PGI2. The treatment of vascular rings with NTG in concentrations of 5 to 1000 ng/ml and subsequent incubation with AA caused a significant increase in PGI2 in the supernatants, as identified by bioassay (platelet aggregation inhibition) and by measurement of 6-keto-PGF1 alpha (stable hydrolysis product of PGI2). The maximum increase in PGI2 was observed with therapeutic concentrations of NTG, i.e., 5 to 10 ng/ml. The levels of vessel wall-generated TXB2 (stable metabolite of TXA2) were not affected by NTG treatment. A prior incubation of vascular rings with indomethacin abolished the increase in PGI2 after NTG treatment. In contrast, incubation of vascular rings with OKY 1581 (selective TXA2 inhibitor) resulted in a significant additional increase in PGI2 release but no change in TXB2 levels after NTG treatment. These studies indicate important effects of NTG on vascular PGI2 generation but not on TXA2 generation.
D011464:Epoprostenol / Q000096:biosynthesis*; D006801:Humans; D007231:Infant, Newborn; D005996:Nitroglycerin / Q000494:pharmacology*; D011453:Prostaglandins / Q000096:biosynthesis*; D012501:Saphenous Vein / Q000187:drug effects* / Q000378:metabolism; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis*; D014471:Umbilical Veins / Q000187:drug effects* / Q000378:metabolism
D011453:Prostaglandins; D013931:Thromboxanes; D013928:Thromboxane A2; D011464:Epoprostenol; D005996:Nitroglycerin