11-Deoxycorticosterone (DOC), or simply deoxycorticosterone, also known as 21-hydroxyprogesterone, as well as desoxycortone (INN), deoxycortone, and cortexone, is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. It is an active (Na+-retaining) mineralocorticoid. As its names indicate, can be understood as the 21-hydroxy-variant of progesterone or as the 11-deoxy-variant of corticosterone. DOCA is the abbreviation for the ester 11-deoxycorticosterone acetate. Biological activity DOC is a potent mineralocorticoid but is virtually devoid of glucocorticoid activity. However, 11β-hydroxylation of DOC produces corticosterone and confers glucocorticoid activity, along with 10-fold reduced mineralocorticoid activity. In addition to its mineralocorticoid activity, DOC has been found to possess one-third to one-tenth the potency of progesterone as a progestogen when administered systematically to rabbits. However, it has no such activity when applied directly to the uterine mucosa of mice. The discrepancy may be related to the fact that DOC can be converted into progesterone in vivo. Biological role DOC is a precursor molecule for the production of aldosterone. The major pathway for aldosterone production is in the adrenal glomerulosa zone of the adrenal gland. It is not a major secretory hormone. It is produced from progesterone by 21β-hydroxylase and is converted to corticosterone by 11β-hydroxylase. Corticosterone is then converted to aldosterone by aldosterone synthase. Most of the DOC is secreted by the zona fasciculata of the adrenal cortex which also secretes cortisol, and a small amount by the zona glomerulosa, which secretes aldosterone. DOC stimulates the collecting tubules (the tubules which branch together to feed the bladder) to continue to excrete potassium in much the same way that aldosterone does but not like aldosterone in the end of the looped tubules (distal). At the same time it is not nearly so rigorous at retaining sodium as aldosterone, more than 20 times less. DOC accounts for only 1% of the sodium retention normally In addition to its inherent lack of vigor there is an escape mechanism controlled by an unknown non steroid hormone which overrides DOC's sodium conserving power after a few days just as aldosterone is overridden also. This hormone may be the peptide hormone kallikrein, which is augmented by DOC and suppressed by aldosterone. If sodium becomes very high, DOC also increases urine flow. DOC has about 1/20 of the sodium retaining power of aldosterone, and is said to be as little as one per cent