1. The excretion rates of renal thromboxane B2 (TXB2) and 6-ketoPGF, the stable chemical metabolites of thromboxane A2(TXA2) and prostaglandin I2 (PGI2) respectively, PGE2 and sodium were determined in normal and saline-loaded rats treated with the thromboxane synthetase inhibitor imidazole.

2. In normal rats the administration of imidazole in doses which did not affect renal 6-keto-PGF and PGE2 excretion but selectively inhibited renal TXB2 excretion, significantly increased the sodium excretion rate.

3. Volume expansion with saline increased renal PGE2 and 6-ketoPGF excretion but did not alter renal TXB2 excretion. The increase in renal prostaglandin excretion was accompanied by an increased sodium excretion rate.

4. The administration of imidazole to saline-loaded animals also decreased renal TXB2 excretion but did not alter the increased excretion of renal PGE2 and 6-ketoPGF. This reduction in renal thromboxane biosynthesis by imidazole further increased the sodium excretion rate.

5. We suggest that TXA2 is a potent anti-natriuretic factor as well as the most potent vasoconstrictor agent known.

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