to unload both excess sodium and potassium. DOC's action in augmenting kallikrein, the peptide hormone thought to be the sodium "escape hormone," and aldosterone's action in suppressing it, is also supportive of the above concept. ACTH has more effect on DOC than it does on aldosterone. This may be to give the immune system control over the electrolyte regulation during diarrhea since during dehydration, aldosterone virtually disappears even though renin and angiotensin rise high. It is because aldosterone disappears that potassium supplements are very dangerous during dehydration and must not be attempted until at least one hour after rehydration so the hormones can reach the nucleus. DOC's primary purpose is to regulate electrolytes. However, it has other effects, such as to remove potassium from leucocytes and muscle, depress glycogen formation and to stimulate copper containing lysyl oxidase enzyme and connective tissue, which attributes may be used by the body to help survive during potassium wasting intestinal diseases. The greater efficiency of DOC in permitting sodium excretion (or perhaps it should be expressed as inefficiency at retention) must be partly through morphological changes in the kidney cells because escape from DOC's sodium retention takes several days to materialize, and when it does, these cells are much more efficient at unloading sodium if sodium is then added than cells accustomed to a prior low intake. Thus, paradoxically, a low salt intake should be protective against loss of sodium in perspiration. Progesterone prevents some of the loss of potassium by DOC. Additional images See also 11-Deoxycortisol 17α-Hydroxyprogesterone Corticosterone Congenital adrenal hyperplasia References Sources Glycine receptor antagonists Mineralocorticoids Pregnanes Progestogens Steroid hormones