Effect of ventilatory rate on renal venous PGE2 and PGF2 alpha efflux in anesthetized dogs

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Abstract
In anesthetized laparotomized male mongrel dogs with ventilatory rate set at 10 breath .cntdot. min-1, tidal volume was adjusted so that control arterial pH and PCO2 [partial pressure of CO2] were within the normal range for unanesthetized dogs. Control renal venous PG[prostaglandin]E2 and PGF2.alpha. concentrations were comparable to those of unanesthetized dogs, namely, 57 .+-. 10 and 114 .+-. 18 pg .cntdot. ml-1, respectively. Control arterial plasma renin activity (PRA), 6.6 .+-. 1.2 ng .cntdot. ml-1 .cntdot. 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 .cntdot. 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.. It may be a more important determinant of resting concentrations of PG in renal venous blood than anesthesia, laparotomy, or PRA.