The induction of thromboxane synthetase as an expression of renal pathology

Arachidonic acid metabolism by intact perfused kidneys or by microsomes prepared from normal rabbit kidneys primarily results in the formation of prostaglandin (PG)E₂. Unilateral ureter obstruction or partial occlusion of the renal vein of rabbits leads to the release of a rabbit aorta contracting substance when such isolated perfused kidneys are stimulated with vasoactive peptides (e.g. angiotensin II and bradykinin). Homogenates of those perfused surgically modified kidneys exhibit the enzymatic conversion of either arachidonic acid or PGH₂ into thromboxane B₂. Radioimmunoassay of the renal venous effluent from the perfused ureter or renal vein obstructed kidneys demonstrated the simultaneous presence of PGE₂, thromboxane A₂, and prostacyclin in extraordinary amounts following peptide stimulation. On the other hand, the contralateral control kidney released low levels of PGE₂ and only trace amounts of thromboxane and PGI₂ when stimulated. Thus, in renal pathological states, arachidonate metabolism results in the simultaneous synthesis of a number of biologically active substances and their interplay must play an intimate role in the ultimate response of this tissue.