The induction of thromboxane synthetase as an expression of renal pathology

P. Needleman, S. Myers, D. F. Reingold, K. Watters, S. Holmberg, A. Wyche, A. R. Morrison

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)111
Number of pages1
JournalProgress in Lipid Research
Issue numberC
StatePublished - 1981


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