![]() ![]() ![]() Renin and potassium levels were normal and comparable in both groups. The other 4 patients had ZG responsive to stimulation with angiotensin III, increasing aldosterone and 18-OHB production significantly (P < 0.025). The administration of cosyntropin (Cortrosyn 250-μg iv bolus) to these same patients, however, effected a significant increase (P < 0.001) in 18-OHB (from 6.6 ± 1.7 to 26.7 ± 2.5 ng/dl) without changing the aldosterone level (5.4 ± 0.6 to 7.0 ± 1.4 ng/dl). Four of these subjects had no aldosterone or 18-OHB response to angiotensin II (des-Asp1-angiotensin II) infusion, indicating suppression of the ZG. Eight patients, previously treated with 100-300 mg spironolactone (Aldactone) daily for an average of 86 days, were studied under metabolically balanced conditions 7-14 days after the removal of one adrenal gland containing an aldosterone-producing adenoma. We studied an additional condition in which the ZG is chronically suppressed to determine if the ZF also produces 18-OHB. In the latter, however, excessive 18-OHB production most likely originates in the ZF. Dissociative production of 18-OHB and aldosterone is only found in patients with the corticosterone-methyl-oxidase type II deficiency or the 17α-hydroxylase deficiency form. Its secretory patterns are closely related to those of aldosterone and usually unrelated to those of cortisol or other zona fasciculata (ZF) steroids. ![]() 18-Hydroxycorticosterone (18-OHB) is produced in the zona glomerulosa (ZG). ![]()
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