The adrenal glands are paired endocrine organs located in the retroperitoneal space. The left adrenal gland is the larger of the pair and is positioned near the craniomedial border of the left kidney; the right adrenal gland is adjacent to the hilus of the right kidney.
Each gland consists of two distinct parts—the outer cortex and the inner medulla—which differ in morphology, function, and origin. Excess or deficiency of adrenal hormones can cause disease.
Adrenal Cortex in Animals
The adrenal cortex is composed of three zones:
The outermost zone (zona glomerulosa) synthesizes and secretes mineralocorticoids.
The middle zone (zona fasciculata) produces glucocorticoids.
The inner zone (zona reticularis) secretes sex steroids.
Mineralocorticoids
Mineralocorticoids, consisting mainly of aldosterone, maintain water and electrolyte balance.
Aldosterone secretion increases in response to hypovolemia and hypotension via the renin-angiotensin-aldosterone system (RAAS), with angiotensin II stimulating aldosterone synthesis and secretion from the adrenal cortex. Hyperkalemia also has a direct stimulatory effect on aldosterone production, and hyponatremia promotes aldosterone release as well.
Aldosterone has various effects in the body:
It acts on the principal cells of the renal tubule to increase sodium and chloride reabsorption and potassium excretion.
It exerts its potassium-excreting and sodium-conserving effects on salivary glands, sweat glands, and the colon, with a net effect of sodium retention and potassium loss.
It affects acid-base status via its action on the intercalated cells of the renal tubule to promote the exchange of hydrogen ions for sodium.
Glucocorticoids
Glucocorticoids are synthesized and secreted under regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Corticotropin-releasing hormone (CRH) is released by the hypothalamus. CRH release stimulates the release of ACTH from the adenohypophysis (ie, anterior pituitary gland). ACTH stimulates the synthesis and release of glucocorticoids from the zona fasciculata. Glucocorticoids inhibit the release of CRH and ACTH via negative feedback on the hypothalamus and pituitary, resulting in balance.
The effects of glucocorticoids (cortisol and corticosterone) are far-reaching in the body:
They are catabolic steroids that antagonize the actions of insulin by increasing gluconeogenesis, mobilizing fatty acids, stimulating muscle catabolism, and preventing the uptake of glucose by muscle and fat.
They stimulate appetite.
They are essential for maintaining normal blood pressure and vascular tone in addition to GI barrier function and motility.
They suppress inflammation, decrease wound healing, and have an overall inhibitory effect on the immune system.
Sex Steroids
Progesterone, estrogens, and androgens are adrenal sex hormones.
Excess secretion of these steroid hormones can be associated with adrenocortical tumors, the clinical signs of which depend on which steroids are secreted in excess. In both pituitary-dependent and adrenal-dependent hyperadrenocorticism, secretion of adrenal sex steroids is increased; the increase is of unknown clinical importance.
A syndrome called occult (or atypical) hyperadrenocorticism has been reported in association with excessive production of adrenal sex steroids. Dogs with this syndrome have clinical signs that suggest Cushing syndrome, but they show normal or low cortisol concentrations after provocative testing. These dogs have increased concentrations of one of several adrenal steroids; however, it is not clear whether the high concentrations of sex hormones are the cause of the clinical signs.
Adrenal Medulla in Animals
The adrenal medulla, the central part of the adrenal gland, is composed of chromaffin cells, which are part of the sympathetic nervous system. The chromaffin cells are stimulated by preganglionic sympathetic neurons and secrete catecholamines.
With the exception of pheochromocytomas, which are adrenal tumors associated with an excess of catecholamines, clinical signs of isolated adrenal medullary disease are very rare. Even in animals with primary hypoadrenocorticism, adrenal medullary function appears to be normal, likely because of extramedullary secretion of catecholamines.
Pheochromocytomas occur in domestic animals, including cattle, dogs, and cats. Typically, older animals are affected. Clinical signs of pheochromocytomas are due to excessive catecholamine secretion or local vascular invasion.
Abdominal CT is the preferred imaging modality for pheochromocytomas because it is the best modality for detecting vascular invasion. Pheochromocytomas and other adrenal medullary tumors are rare and often are detected as an incidental adrenal mass during abdominal imaging for an unrelated reason or at necropsy.
Other adrenal tumors, such as neuroblastomas and ganglioneuromas, can arise in the chromaffin cells.
For More Information
Boron WF, Boulpaep EL. Medical Physiology: A Cellular and Molecular Approach. Updated 2nd ed. Saunders/Elsevier; 2012.
Ritter J, Flower RJ, Henderson G, et al. Rang and Dale’s Pharmacology. 10th ed. Elsevier; 2024.
Behrend, EN. Canine hyperadrenocorticism. In Feldman EC, Nelson RW, Reusch C, Scott-Moncrieff, JCR. Canine & Feline Endocrinology. 4th ed. Elsevier Saunders; 2015:377-451.
Also see pet health content regarding disorders of the adrenal glands in dogs and cats.
