1. Intravenous frusemide produced in normal subjects a prompt rise of plasma renin concentration which correlated with urinary sodium.
2. The renin response to frusemide was suppressed in patients with primary hyperaldosteronism.
3. In patients with low-renin hypertension and normal renin essential hypertension, the renin response to frusemide was similarly suppressed.
4. Suppression of the renin response to frusemide is therefore a feature of hypertension not confined to patients with primary hyperaldosteronism and low-renin hypertension.
5. Thus low-renin hypertension does not appear to constitute a distinct diagnostic entity.
6. It is suggested that suppression of the renin response is part of a long-term renal adaptation to high blood pressure.