these results indicate that the natriuresis and antihypertensive effect of furosemide in vivo , which is associated with a significant increase in urinary pge2 , is not the result of a direct stimulation of furosemide on prostaglandin synthesis but may result from a decrease in pge metabolism , conversion to another biologically active prostaglandin or possibly be a reflection of events secondary to a direct effect of furosemide on renal hemodynamics and electrolyte excretion .
C0025519
metabolism
C0221102
excretion