1. The effects of microcrystalline ‘depot’ triamcinolone acetonide on renal excretion and blood levels of aldosterone, 18-hydroxycorticosterone and corticosterone were studied in rats over a 13 day period. The renal excretion of all of these steroids was found to be suppressed on day 1 after triamcinolone acetonide administration. Corticosterone excretion remained suppressed for 6 days, whereas aldosterone and 18-hydroxycorticosterone excretion normalized within 3 days.

2. While corticosterone excretion was returning to control values, the excretion of aldosterone rose to values above the pretreatment levels (the rebound phenomenon). 18-Hydroxycorticosterone excretion paralleled that of aldosterone, but the rebound was of less statistical significance.

3. The findings in urine were confirmed by plasma steroid determinations. A suppression of plasma aldosterone, 18-hydroxycorticosterone and corticosterone was observed in the first 24 h after triamcinolone acetonide injection. On day 4 only corticosterone showed lowered levels. An aldosterone rebound could be seen at 18.00 hours, the circadian maximum in rats.

4. These findings suggest that in addition to the effects on glucocorticoids, mineralocorticoids have to be taken into account in the restoration of the adrenal function after corticoid therapy. The aldosterone rebound observed during this sensitive period may be important in preventing disturbances of electrolyte and water homoeostasis.

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