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1 In eight normotensive male volunteers indomethacin decreased both the peak urine flow rate and total sodium excreted within 1 h of an intravenous dose of frusemide.2 Resting effective renal plasma flow and glomerular filtration rate were unchanged by indomethacin, but the increase in both parameters after frusemide was inhibited.3 The early increase in plasma renin activity after frusemide was inhibited by indomethacin. 4 Indomethacin decreased urinary excretion of PGE by 80% and the increase after frusemide was abolished. 5 The urinary excretion of a metabolite of systemic PGI2was unaltered in the 40-60 min period following frusemide.6 The early haemodynamic effects of frusemide are likely to be prostaglandin mediated, but there was no evidence of any change in systemic PGI2 synthesis after frusemide.

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Methods: A total of 135 eligible patients were identified, of whom 55 (44%) were randomised. Eligible patients had sustained hypertension, with a minimum diastolic BP of 95 mm Hg on at least two anti-hypertensive drugs. Renal artery stenosis was defined by renal angiography as at least 50% stenosis in the affected vessel. All patients were observed during an initial 4-week run-in period on a fixed drug regimen and subsequent changes measured from this 4-week baseline. Results: Blood pressure fell during the run-in period in all groups. In patients with bilateral renal artery stenosis randomised to angioplasty, a statistically significant (P Ͻ 0.05) fall in BP was observed at latest follow-up (range 3-54 months). The mean fall in BP at latest follow-