Selective inhibition of thromboxane synthesis in glycerol-induced acute renal failure.
It has recently been postulated that thromboxane A2 may participate in the pathogenesis of acute myohemoglobinuric experimental acute renal failure. To investigate this further, the effect of selective inhibition of thromboxane synthesis on the course of glycerol-induced acute renal failure was determined. Despite significant inhibition of thromboxane synthesis by 4-imidazole-yl-acetophenone, the functional and morphologic disturbance induced by glycerol was unaltered. Moreover, pretreatment with 4-imidazole-yl-acetophenone failed to prevent the fall in renal blood flow seen following glycerol administration. These results argue against a major role for thromboxane A2 in the pathogenesis of this form of experimental acute renal failure.
D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis; D058186:Acute Kidney Injury / Q000139:chemically induced / Q000378:metabolism*; D000818:Animals; D005990:Glycerol / Q000037:antagonists & inhibitors*; D007093:Imidazoles / Q000494:pharmacology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation / Q000187:drug effects; D013931:Thromboxanes / Q000096:biosynthesis* / Q000097:blood; D014655:Vascular Resistance / Q000187:drug effects
D007093:Imidazoles; D013931:Thromboxanes; C034480:Ro 22-3581; D015121:6-Ketoprostaglandin F1 alpha; D005990:Glycerol