Potentiating effects of leukotriene B4 and prostaglandin E2 on urinary sodium excretion by the dog kidney.

A synergistic vasodilatation was recently demonstrated with leukotriene B4 (LTB4) and prostaglandin E2 (PGE2) in the cutaneous microcirculation. The present study addresses this question to the renal microcirculation, with respect to its eventual influence on the net transport of sodium, infusing small doses of LTB4 (100 ng/min) and PGE2 (3 ng/min) in the left renal artery, and using the contralateral kidney as control in anesthetized Mongrel dogs. In group 1 (hydropenic animals), LTB4 alone failed to influence natriuresis (UNaV) while PGE2 increased UNaV from 152 +/- 20 to 225 +/- 18 uEq/min. The combined infusion of LTB4 and PGE2 resulted in a marked elevation of natriuresis to 368 +/- 26, 317 +/- 30 and 342 +/- 52 uEq/min. In group 2, water diuresis was induced to examine the eventual site of action of these compounds, and to assess the response of the diluting segment of the nephron. In these dogs, PGE2 was first administered and UNaV rose modestly from 51 +/- 12 to 77 +/- 15 uEq/min. LTB4 again had no significant influence on UNaV, but LTB4 and PGE2 produced a marked increment from 75 +/- 16 to 374 +/- 24 uEq/min. Urine volume, as well as free water clearance, increased from 3.3 +/- 0.2 to 6.5 +/- 0.7 ml/min, and from 2.3 +/- 0.2 to 3.7 +/- 0.4 ml/min, respectively, during LTB4 + PGE2. No significant change occurred in the right control kidney during these manoeuvers. Since renal hemodynamics (glomerular filtration and plasma flow) remained relatively stable in both groups of dogs, it is suggested that the combined infusion of LTB4 and PGE2 exerts a direct influence on the net transport of sodium, probably in the proximal tubule, as inferred by the results obtained in group 2. These two important metabolites of arachidonic acid could be involved in the modulation of renal sodium excretion under normal and/or pathophysiological conditions.