The adrenal cortex is subdivided into 3 layers or zones, although the demarcation between zones often is indistinct. The zona glomerulosa (multiformis), 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 hyperglycaemia and increased glucose production. In addition, they decrease lipogenesis and increase lipolysis 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 favours 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 can have a profound negative effect on wound healing. High therapeutic levels 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.
The adrenal medulla, although apparently not essential to life, plays an important role in response to stress or hypoglycaemia. It secretes epinephrine and norepinephrine, which increase cardiac output, blood pressure, and blood glucose, and decrease GI activity.
A pheochromocytoma can develop in any mammal. These tumours are unusual in that they secrete epinephrine (adrenalin), norepinephrine (noradrenalin), or both. Clinical signs are often absent, and tumors may be incidental findings during the workup for other conditions or at necropsy. In some dogs, clinical signs may include polyuria, polydipsia, tachycardia, restlessness, abdominal distension, and collapse. Due to the lack of routine availability of validated assays for catecholamines in dogs and cats, the diagnosis is often made on the basis of clinical signs and ultrasound. Treatment involves surgery (if feasible) and management of hypertension. Other adrenal tumors, such as neuroblastomas and ganglioneuromas, may arise in the chromaffin cells of the sympathetic nervous system.