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The adrenal gland is a complex organ chiefly responsible for the secretion of cortical steroids necessary for the stress response. It is also known as the “suprarenal gland” as it is located above the kidneys in the retroperitoneal space surrounded by an adipose capsule and renal fascia.


The adrenal gland is split into two main zones, cortex and medulla, both of which produce hormones. Interestingly, the right adrenal gland is triangular in shape, whereas the left adrenal gland is semilunar in shape. Furthermore, the mechanism for secreting these hormones differs between the two zones.

The cortex is further subdivided into three layers, from superficial to deep:

  • The Zona Glomerulosa is the primary site for aldosterone production. Aldosterone is an important mineralocorticoid that is essential for long-term regulation of blood pressure.

  • The Zona Fasciculata is responsible for production of glucocorticoids, such as 11-deoxycorticosterone, corticosterone, and cortisol.

  • The Zona Reticularis produces androgens, such as dehydroepiandosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (which eventually becomes testosterone). It receives its neuroendocrine hormonal control from the hypothalamic–pituitary axis (HPA), especially the hypothalamus, in addition to the renin–angiotensin–aldosterone system (RAAS).

The medulla produces the body’s primary source of circulating catecholamines (CA), which as we know is immensely important in the fight-or-flight response. CA release is stimulated by a variety of events, including exercise, surgery, hemorrhage, hypotension, hypoglycemia, hypercapnia, hypothermia, pain, and hypoxemia. It differentially secretes ~80% epinephrine, and ~20% norepinephrine, in addition to small amounts of dopamine. Differing from the adrenal cortex, the medulla receives its input from the sympathetic nervous system through preganglionic fibers, where it releases its secretions directly into the blood stream via an endocrine or neuroendocrine signaling mechanism. The cortisol produced in the adrenal cortex diffuses into the medulla, and with high levels increases epinephrine production and secretion via a paracrine mechanism. The adrenal androgens have minimal clinical relevance to anesthetic management, and for the sake of the discussion will not be further explored.

The mineralocorticoid aldosterone is chiefly involved with fluid and electrolyte balancing within the body. Principally, the RAAS (specifically Angiotensin II), ACTH, and hyperkalemia are responsible for an increase production of aldosterone. Furthermore CHF, hypovolemia, hypotension, and surgery can upregulate production of this hormone. Aldosterone secretion acts on the sodium–potassium pumps in the distal convoluted tubule, permitting sodium reabsorption, in exchange for potassium and hydrogen excretion. Its net effect is volume expansion via fluid retention, with a reduction in potassium and hydrogen ions. Thus, an excess of aldosterone will create volume expansion, hypertension, hypokalemia, and metabolic acidosis. Importantly, treatment of conditions such as CHF and hypertension takes advantage of this pathway by blocking the RAAS, and thus aldosterone production, which is accomplished via an angiotensin converting enzyme inhibitor (ACEi) or an angiotensin receptor blocker (ARB). The aldosterone receptor blockers, such as spironolactone or eplerenone, further increase survival ...

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