Accompanying the arterial hypertension in the dog following the partial constriction of one of a pair of renal arteries, there are rises in plasma renin activity, plasma volume and renal venous prostaglandins E and F of the contralateral kidney, reaching maxima on days 2, k and 5 respectively. By the tenth day all parameters were normal, with the exception of blood pressure. It is suggested that the contralateral kidney responds to the fluid retention by natriuresis and diuresis mediated by an increase in prostaglandin synthesis. It is also concluded that PGE is unlikely to play a role in the antihypertensive action of this kidney. A transient elevation of circulating PGA was observed in some experiments. In the two-kidney Goldblatt rat a transient decrease in renal plasma flow of the clipped kidney was seen whilst the contralateral kidney showed no change. Renal venous PC-E2 and PGF2CK concentrations changed inversely with renal plasma flow and calculated secretion rate of the clipped kidney fell, although it was not possible to establish the significance of this fall. Such a fall could lead to a reduction in intrarenal vasoconstrictor potentiation produced by prostaglandins in this species. The absence of a rise in secretion rate of PGE2 in either kidney raises further doubt concerning renal prostaglandins as mediators of the antihypertensive action of the kidney in the rat. In the pump-perfused dog kidney calculated secretion rate of PGE fell as perfusion pressure fell below the autoregulation range, whilst PGF secretion did not change. Meclofenamate failed to abolish renal blood flow autoregulation, despite a 70% fall in prostaglandin synthesis and it is therefore concluded that autoregulation is not dependent on prostaglandins.