The role of TXA2 in hypertension.
Blood pressure reduction induced by antihypertensive drugs with different mode of action approximated the pathological altered synthesis of TXB2 in spontaneously hypertensive rats to values of normotensive rats: in the kidney medulla by all drugs used, in the aorta only by the most efficient drugs (clonidine, dihydralazine) and in plasma and serum only in connection with a reduction in heart rate (clonidine, propranolol). The pathologically increased synthesis of 6-keto-PGF1 alpha was unchanged by drugs, therefore the ratio PGI2/TXA2 was directed towards the vasodilatory prostanoid. Unlike SHR in NTR an equieffective blood pressure reduction induced by the same drugs was without influence on TXB2 synthesis. From these results we can conclude, that the influence of antihypertensive drugs on TXB2 synthesis depends on the normotensive or hypertensive state of the animals and not on the drug per se. In hypertensive patients a blood pressure reduction by linseed oil was connected with a reduced TXB2 plasma level, too.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D001011:Aorta / Q000378:metabolism; D001794:Blood Pressure / Q000187:drug effects*; D003000:Clonidine / Q000494:pharmacology; D004078:Dihydralazine / Q000494:pharmacology; D006973:Hypertension / Q000503:physiopathology*; D007679:Kidney Medulla / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D011919:Rats, Inbred Strains; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis*; D014192:Trapidil / Q000494:pharmacology
D000959:Antihypertensive Agents; D013931:Thromboxanes; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011433:Propranolol; D014192:Trapidil; D003000:Clonidine; D004078:Dihydralazine