Renal blood flow autoregulation was studied in anaesthetized greyhounds, using an electromagnetic flowmeter, before and after the administration of the prostaglandin-synthesis inhibitor, indomethacin, or phosphate buffer. 2. Indomethacin caused a reduction in renal blood flow at all levels of perfusion pressure, but did not affect the ability of the kidney to autoregulate. 3. The aburpt reinstatement of renal perfusion pressure from previously reduced levels caused a triphasic transient response in flow. Peak hyperaemia at the beginning of the transient was not affected by indomethacin. After indomethacin, the second phase of this flow transient showed an oscillatory pattern during which flow fell initially to levels significantly lower than control. 4. It is concluded that although indomethacin did not abolish steady-state autoregulation, renal prostaglandins may damp rapid oscillations in renal blood flow and thus contribute to the efficiency of autoregulation.
