Urinary immunoreactive PGA and PGE, plasma and urinary aldosterone, and plasma renin activity (PRA) were determined in eleven control subjects and four patients with diabetic hyporeninaemic hypoaldosteronism (HH) before and during 4 days of sodium chloride restriction and frusemide administration. Aldosterone and PRA increased steadily in control subjects, but not in patients with HH. Increases in urinary PGA and PGE were observed during volume depletion. The basal levels and increases observed were comparable in both groups. The apparently normal stimulation of PGA and PGE in subjects with diabetic HH suggests that this syndrome is not associated with abnormal prostaglandin metabolism, despite the fact that drug‐induced abnormalities of the latter may precipitate or aggravate the clinical syndrome in susceptible individuals. The increase in PGA and PGE following frusemide treatment and salt depletion supports the possibility of a relationship between renal prostaglandin metabolism, frusemide‐induced natriuresis and/or renin secretion. While the nature of this relationship remains obscure, the increases in PGA and PGE in the absence of increases in renin‐angiotensin levels in subjects with HH suggests that these changes are not due to activation of the renin‐angiotensin system.