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1. Highly specific antibodies to human renin were prepared in rabbits and used for the preparation of a renin-free substrate, the direct radioimmunoassay of renin in plasma and kidneys, and the localization of renin with fluoresceinated antibodies. 2. In a patient with a partially infarcted kidney, plasma renin activity was increased, and could be activated by acid. The direct measurement of plasma renin by radioimmunoassay gave identical values before and after acidification. 3. In the ischaemic part of the kidney, renin content was high, both by the enzymatic and the direct method of measurement. It was low in the non-ischaemic part of the kidney. 4. All afferent and some interlobular arteries of the obsolescent glomeruli were stained with fluoresceinated anti-renin antibodies. In the non-ischaemic area, the juxtaglomerular apparatus did not stain. 5. Renin can now be measured in human plasma and kidney as an entity, by a specific radioimmunoassay. A direct investigation of this intrarenal hormone is now possible at the renal tissue level.

1. Acute renal failure was induced in conscious rats by subcutaneous injection of glycerol. 2. Expansion of the extracellular space by infusion of 150 mmol/l sodium chloride (saline) partly protected the animals against acute renal failure. 3. This protective effect of saline infusion disappeared when the animals were treated with indomethacin. This effect could be reversed by the addition of prostaglandin (PGE2) to the saline infusion. 4. We suggest that prostaglandins may be involved in mediating the protection afforded by saline infusion against acute renal failure due to glycerol.

1. Renal venous prostaglandin concentrations (PGA, PGE and PGF) were determined, together with renal plasma flow, urinary output and blood pressure changes, before and after infusion of sodium chloride solution (saline) in four normotensive and three hypertensive subjects. 2. No changes in blood pressure and in glomerular filtration rate were observed. 3. Saline infusion induced a significant increase in renal venous PGA and PGE, and also in total and non-cortical renal plasma flow and urinary output. There was an insignificant increase in renal venous PGF. 4. These findings show that prostaglandin release after saline infusion is associated with changes in renal blood flow and suggest that the natriuretic and diuretic effect of saline could be the result of prostaglandin release.

1. The excretion rates of renal thromboxane B2 (TXB2) and 6-ketoPGF1α, 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-PGF1α 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-ketoPGF1α 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-ketoPGF1α. 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.