Hypoxia inhibits renal thromboxane and not prostacyclin release

The effect of hypoxia on renal prostanoid synthesis and renal function was studied. The kidneys of male Sprague-Dawley rats were cannulated and perfused in vitro with Krebs-Henseleit buffer with a pO2 of 460 (control) or 60 mm torr (hypoxia). The rate of perfusion was adjusted to maintain perfusion pressure at 100 mm Hg. The renal venous effluent was collected at 15, 30, 60, 120, 150, and 180 min and assayed for basal release of 6-keto-PGF1 alpha, PGE2, and thromboxane B2 by radioimmunoassay and inulin and sodium clearance. Prostanoid release was high at 15 min, decreased to a lower level up to 120 min, and then progressively increased after 150 min of perfusion. Hypoxia significantly decreased TxB2 release at 30, 60, 150, and at 180 min but not PGE2 or 6-keto-PGF1 alpha release. Hypoxia proportionally decreased both sodium and inulin clearances suggesting that the decrease in renal function was from decreased renal flow. The kidney responded to the altered renal function by increasing the ratio of vasodilator to vasoconstrictor prostanoids by inhibition of TxB2 release.