Effect of furosemide on prostacyclin-like antiaggregatory release from vessel wall and renal cortex

Abstract

Summary In the present study prostacyclin is discussed as a possible mediator of intra- and extrarenal activities of furosemide. Compared to controls the aortas from rats treated with therapeutical doses of furosemide show ex vivo a significantly higher release of acid labile PGI 2 -like antiaggregatory activity, which can be suppressed by pre-treatment of the rats with indomethacin or acetylsalicyclic acid. However, furosemide does not stimulate PGI 2 -like release from rat aortas in vitro. Furthermore, inhibition of induced aggregation of human platelets in vitro is rather weak requiring high concentrations of furosemide. Apparently, there is no direct site of action of furosemide, regarding anti-platelet activity or PGI 2 -release from vessel wall. Instead, furosemide seems to enhance PGI 2 -release from vessel walls via secondary factors present in plasma after in vivo administration. The enhanced PGI 2 then might exert valuable extrarenal effects, like preventing the formation of platelet thrombi as well as hypertension in patients. The antiaggregatory activity, present in supernatants of renal cortical slices, was not altered after treatment of the rats with furosemide in our experiments.