The adrenal cortex is subdivided into 3 layers or zones, although the demarcation between zones often is indistinct. The zona glomerulosa, the outer zone, is responsible for the secretion of mineralocorticoid hormones. The zona fasciculata, the middle zone, comprises ~70% of the cortex and is composed of cells that contain abundant cytoplasmic lipid and the glucocorticoid hormones. The zona reticularis, the inner zone, is responsible for the secretion of sex steroids.
Mineralocorticoids, of which the most potent naturally occurring one is aldosterone, are adrenal steroids that have their principal effects on ion transport by epithelial cells, resulting in a loss of potassium and retention of sodium. Sweat glands and the electrolyte “pumps” in epithelial cells of the renal tubule respond similarly. In the distal convoluted tubule of the mammalian nephron, a cation-exchange mechanism resorbs sodium from the glomerular filtrate and secretes potassium into the lumen. These reactions are accelerated by mineralocorticoids and proceed more slowly in their absence. A lack of secretion of mineralocorticoids (Addison's disease) may result in a lethal retention of potassium and loss of sodium.
Cortisol and lesser amounts of corticosterone are the most important glucocorticoid hormones secreted by the adrenal gland in many species. In general, the actions of glucocorticoids on carbohydrate, protein, and lipid metabolism result in sparing of glucose and a tendency to hyperglycemia and increased glucose production. In addition, they decrease lipogenesis and increase lipol-ysis in adipose tissue, which results in release of glycerol and free fatty acids.
Glucocorticoids also suppress inflammatory and immunologic responses, thereby attenuating associated tissue destruction and fibroplasia. However, high levels of glucocorticoids reduce resistance to bacteria, viruses, and fungi, which favors the spread of infection. Glucocorticoids may impair the immunologic response at any stage from the initial interaction and processing of antigens by cells of the reticuloendothelial system, through the induction and proliferation of immunocompetent lymphocytes and subsequent antibody production. Inhibition of a number of lymphocyte functions forms part of the basis for immunosuppression.
Glucocorticoids may have a profound negative effect on wound healing. High therapeutic doses of adrenal corticosteroids or the syndrome of hyperadrenocorticism may cause wound dehiscence after surgery. The inhibition of fibroblast proliferation and collagen synthesis leads to a decrease in scar tissue formation.
Progesterone, estrogens, and androgens are adrenal sex hormones. Excess secretion may be associated with a neoplasm of the zona reticularis. The manifestation of virilism, precocious sexual development, or feminization depends on which steroid is secreted in excess, sex of the individual, and age of onset. In addition, a syndrome termed atypical hyperadrenocorticism has been reported in association with excessive production of adrenal sex steroids. The symptoms mirror those of Cushing's syndrome (see The Pituitary Gland: Hyperadrenocorticism), despite normal or low levels of cortisol concentrations following provocative testing. Dogs with this syndrome have elevated concentrations of one of several adrenal steroids, which lead to the clinical signs. Treatment options are similar to those used in the management of Cushing's syndrome.
Last full review/revision July 2011 by David Bruyette, DVM, DACVIM