The maintenance of normal basal secretion and the ability to produce a stress-induced rise in cortisol secretion are critical to homeostasis. Glucocorticoids have a multiplicity of effects, among which are maintenance of glucose homeostasis, facilitation of free water clearance, and maintenance of vascular tone. Patients with glucocorticoid deficiency manifest hypotension which is resistant to the effects of volume expansion and vasopressors. This form of hypotension has been attributed to (1) renin substrate deficiency, (2) a direct effect of glucocorticoids, and/or (3) the lack of cortisol inhibition of nitric oxide and/or prostaglandin I2 synthesis, both potent vasodilators.1,2

At birth, complex changes occur in both the secretion and metabolism of steroids; these result in maintenance of appropriate postnatal cortisol production.3

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