In anesthetized laparotomized male mongrel dogs with ventilatory rate set at 10 breath.min-1, tidal volume was adjusted so that control arterial pH and PCO2 were within the normal range for unanesthetized dogs. Control renal venous PGE2 and PGF2 alpha concentrations were comparable to those of unanesthetized dogs, namely, 57 +/- 10 and 114 +/- 18 pg.ml-1, respectively. In contrast, control arterial plasma renin activity (PRA), 6.6 +/- 1.2 ng.ml-1.h-1, was considerably greater than in unanesthetized dogs. Stepwise increases in ventilatory rate increased renal venous PGE2 and PGF2 alpha to 109 +/- 18 and 205 +/- 41 pg.ml-1, respectively. Hyperventilation reduced PCO2 and increased pH and PRA but had no effect on renal blood flow, arterial blood pressure, or arterial PGE2 and PGF2 alpha concentrations. When the ventilatory rate was returned to control levels, pH, PCO2, PRA, and renal venous PGE2 and PGF2 alpha concentrations returned to control. Ventilatory rate or some consequence of altering ventilatory rate is, therefore, a determinant of renal venous efflux of PGE2 and PGF2 alpha. Moreover, it may be a more important determinant of "resting" concentrations of prostaglandins in renal venous blood than anesthesia, laparotomy, or PRA.