SummaryThe effect of confectionery liquorice on electrolyte status and the renin-angiotensin-aldosterone (RAA) axis was studied in 14 healthy volunteers. They ate liquorice in daily doses of 100 g or 200 g (equivalent to 0 7-14 g glycyrrhizinic acid) for one to four weeks.Plasma potassium concentrations fell by over 03 mmol/l in 11 people, including four who had to be withdrawn from the study because of hypokalaemia. One or more values of the RAA axis, especially plasma renin activity and urinary aldosterone concentrations, were considerably depressed in all subjects. These results show that potentially serious metabolic effects may occur in some people who eat modest amounts of liquorice daily for less than a week.

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S U M M A R Y1. Plasma aldosterone concentration and urine aldosterone excretion were studied before and during sustained diuresis in six patients with gross congestive heart failure, under conditions of fixed sodium and potassium intake and strict control of body posture. Simultaneous measurements of plasma renin activity, plasma corticotrophin and electrolytes were made to assess the relative importance of these factors in the regulation of aldosterone secretion before and during treatment of congestive heart failure.2. During the pre-treatment phase aldosterone levels were normal or raised, but with acute diuresis fell to unmeasurable levels in most cases. This depression in aldosterone tended to coincide with peak natriuresis. Later in the diuretic phase aldosterone values increased often to very high levels as dry body weight was attained.3. With few exceptions plasma renin activity fluctuations paralleled those of plasma aldosterone, whereas corticotrophin levels remained largely within normal limits and plasma electrolytes did not change appreciably.4. The results suggest that the renin-angiotensin system is the important regulator of aldosterone secretion before and during diuretic treatment in patients with gross congestive heart failure.

The renin-angiotensin-aldosterone system and electrolyte levels in 11 patients with heartfailure controlled on digoxin and frusemide were investigated after separate periods of Slow K, spironolactone, and amiloride therapy. When spironolactone or amiloride replaced Slow K, distinct parallel increments in the levels of renin, angiotensin II, and aldosterone resulted. Though plasma potassium was generally higher after spironolactone and amiloride than after Slow K, exchangeable potassium was similar with the three regimens. There was no significant relation between plasma potassium and concurrent exchangeable potassium.

The finding that urine cortisol excretion was increased in patients with hypokalaemic hypertension induced by licorice addiction led to this study on the effect of licorice in normal subjects. Thirteen normal volunteers ate either 100 or 200 g licorice for 1-4 weeks and assessment of pituitary-adrenal function was made before, during, and 1 week after cessation of licorice ingestion. Urine cortisol excretion more than doubled in 10 of 13 subjects (mean, 33.8 +/- 15.6 SD before and 83.3 +/- 56 SD micrograms/24 h at 1 week after commencing licorice) and excretion rates similar to those observed in Cushing's syndrome were seen in 7 subjects (range, 91-226, compared to normal range of 11-82 micrograms/24 h). Urine cortisol excretion remained significantly elevated (P less than 0.01) above control levels for at least 1 week after licorice was withdrawn. Despite these increases, urinary steroid metabolite (tetrahydrocortisol, tetrahydrocortisone, tetrahydro-11-deoxycortisol, 17-ketogenicsteroids, and 17-ketosteroids) excretion was not affected, plasma cortisol and ACTH values were unchanged, and normal 0800-1600-h diurnal variation of plasma cortisol was maintained. The direct intraadrenal infusion of the active mineralocorticoid component of licorice, glycyrrhetinic acid, in two sheep with autotransplanted adrenal glands failed to stimulate cortisol secretion acutely. It is concluded from these studies that the licorice-induced changes in cortisol excretion are not a result of adrenocoritcal stimulation but more likely represent a change in the renal handling of cortisol.