The Human Adrenal Cortex: Pathology and Biology — An Integrated Approach

The Human Adrenal Cortex Pathology And Biology An Integrated Approach

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Cortisol is not evenly released during the day — its concentrations in the blood are highest in the early morning and lowest in the evening as a result of the circadian rhythm of ACTH secretion. All corticosteroid hormones share cholesterol as a common precursor. Therefore, the first step in steroidogenesis is cholesterol uptake or synthesis. Cells that produce steroid hormones can acquire cholesterol through two paths. The main source is through dietary cholesterol transported via the blood as cholesterol esters within low density lipoproteins LDL.

LDL enters the cells through receptor-mediated endocytosis. The other source of cholesterol is synthesis in the cell's endoplasmic reticulum. Synthesis can compensate when LDL levels are abnormally low. The initial part of conversion of cholesterol into steroid hormones involves a number of enzymes of the cytochrome P family that are located in the inner membrane of mitochondria. Transport of cholesterol from the outer to the inner membrane is facilitated by steroidogenic acute regulatory protein and is the rate-limiting step of steroid synthesis.

The layers of the adrenal gland differ by function, with each layer having distinct enzymes that produce different hormones from a common precursor. After the production of pregnenolone, specific enzymes of each cortical layer further modify it. Enzymes involved in this process include both mitochondrial and microsomal Ps and hydroxysteroid dehydrogenases.

Usually a number of intermediate steps in which pregnenolone is modified several times are required to form the functional hormones. For example, the most common form of congenital adrenal hyperplasia develops as a result of deficiency of hydroxylase , an enzyme involved in an intermediate step of cortisol production. Glucocorticoids are under the regulatory influence of the hypothalamus-pituitary-adrenal HPA axis.

Glucocorticoid synthesis is stimulated by adrenocorticotropic hormone ACTH , a hormone released into the bloodstream by the anterior pituitary. In turn, production of ACTH is stimulated by the presence of corticotropin-releasing hormone CRH , which is released by neurons of the hypothalamus. The HPA axis also interacts with the immune system through increased secretion of ACTH at the presence of certain molecules of the inflammatory response. Mineralocorticoid secretion is regulated mainly by the renin—angiotensin—aldosterone system RAAS , the concentration of potassium , and to a lesser extent the concentration of ACTH.

Angiotensin receptors in cells of the zona glomerulosa recognize the substance, and upon binding they stimulate the release of aldosterone. Primarily referred to in the United States as epinephrine and norepinephrine , adrenaline and noradrenaline are catecholamines , water-soluble compounds that have a structure made of a catechol group and an amine group.

The adrenal glands are responsible for most of the adrenaline that circulates in the body, but only for a small amount of circulating noradrenaline. Adrenaline and noradrenaline act at adrenoreceptors throughout the body, with effects that include an increase in blood pressure and heart rate. Catecholamines are produced in chromaffin cells in the medulla of the adrenal gland, from tyrosine , a non-essential amino acid derived from food or produced from phenylalanine in the liver. The enzyme tyrosine hydroxylase converts tyrosine to L-DOPA in the first step of catecholamine synthesis.

L-DOPA is then converted to dopamine before it can be turned into noradrenaline. In the cytosol , noradrenaline is converted to epinephrine by the enzyme phenylethanolamine N-methyltransferase PNMT and stored in granules. Glucocorticoids produced in the adrenal cortex stimulate the synthesis of catecholamines by increasing the levels of tyrosine hydroxylase and PNMT.

Catecholamine release is stimulated by the activation of the sympathetic nervous system. Splanchnic nerves of the sympathetic nervous system innervate the medulla of the adrenal gland. When activated, it evokes the release of catecholamines from the storage granules by stimulating the opening of calcium channels in the cell membrane. Cells in zona reticularis of the adrenal glands produce male sex hormones, or androgens , the most important of which is DHEA.

In general, these hormones do not have an overall effect in the male body, and are converted to more potent androgens such as testosterone and DHT or to estrogens female sex hormones in the gonads , acting in this way as a metabolic intermediate. The adrenal gland specific genes with highest level of expression include members of the cytochrome P superfamily of enzymes. The adrenal glands are composed of two heterogenous types of tissue. In the center is the adrenal medulla , which produces adrenaline and noradrenaline and releases them into the bloodstream, as part of the sympathetic nervous system.

Surrounding the medulla is the cortex , which produces a variety of steroid hormones. These tissues come from different embryological precursors and have distinct prenatal development paths. The cortex of the adrenal gland is derived from mesoderm , whereas the medulla is derived from the neural crest , which is of ectodermal origin. The adrenal glands in a newborn baby are much larger as a proportion of the body size than in an adult. The size of the glands decreases relatively after birth, mainly because of shrinkage of the cortex.

The cortex, which almost completely disappears by age 1, develops again from age 4—5. The glands weigh about 1 g at birth [12] and develop to an adult weight of about 4 grams each. Adrenal cortex tissue is derived from the intermediate mesoderm. It first appears 33 days after fertilisation , shows steroid hormone production capabilities by the eighth week and undergoes rapid growth during the first trimester of pregnancy.

The fetal adrenal cortex is different from its adult counterpart, as it is composed of two distinct zones: The fetal zone produces large amounts of adrenal androgens male sex hormones that are used by the placenta for estrogen biosynthesis. The adrenal gland decreases in size after birth because of the rapid disappearance of the fetal zone, with a corresponding decrease in androgen secretion.

During early childhood androgen synthesis and secretion remain low, but several years before puberty from 6—8 years of age changes occur in both anatomical and functional aspects of cortical androgen production that lead to increased secretion of the steroids DHEA and DHEA-S. These changes are part of a process called adrenarche , which has only been described in humans and some other primates. Adrenarche is independent of ACTH or gonadotropins and correlates with a progressive thickening of the zona reticularis layer of the cortex.

Functionally, adrenarche provides a source of androgens for the development of axillary and pubic hair before the beginning of puberty. The adrenal medulla is derived from neural crest cells , which come from the ectoderm layer of the embryo. These cells migrate from their initial position and aggregate in the vicinity of the dorsal aorta , a primitive blood vessel, which activates the differentiation of these cells through the release of proteins known as BMPs.

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These cells then undergo a second migration from the dorsal aorta to form the adrenal medulla and other organs of the sympathetic nervous system. Glucocorticoids produced in the adrenal cortex were once thought to be responsible for the differentiation of chromaffin cells. More recent research suggests that BMP-4 secreted in adrenal tissue is the main responsible for this, and that glucocorticoids only play a role in the subsequent development of the cells. The normal function of the adrenal gland may be impaired by conditions such as infections, tumors, genetic disorders and autoimmune diseases , or as a side effect of medical therapy.

These disorders affect the gland either directly as with infections or autoimmune diseases or as a result of the dysregulation of hormone production as in some types of Cushing's syndrome leading to an excess or insufficiency of adrenal hormones and the related symptoms. Cushing's syndrome is the manifestation of glucocorticoid excess.

It can be the result of a prolonged treatment with glucocorticoids or be caused by an underlying disease which produces alterations in the HPA axis or the production of cortisol. The most common cause of endogenous Cushing's syndrome is a pituitary adenoma which causes an excessive production of ACTH. The disease produces a wide variety of signs and symptoms which include obesity, diabetes, increased blood pressure, excessive body hair hirsutism , osteoporosis , depression, and most distinctively, stretch marks in the skin, caused by its progressive thinning.

When the zona glomerulosa produces excess aldosterone , the result is primary aldosteronism. Causes for this condition are bilateral hyperplasia excessive tissue growth of the glands, or aldosterone-producing adenomas a condition called Conn's syndrome. Primary aldosteronism produces hypertension and electrolyte imbalance, increasing potassium depletion and sodium retention. Adrenal insufficiency the deficiency of glucocorticoids occurs in about 5 in 10, in the general population. If a problem that affects the hypothalamic-pituitary-adrenal axis arises outside the gland, it is a secondary adrenal insufficiency.

Addison's disease refers to primary hypoadrenalism, which is a deficiency in glucocorticoid and mineralocorticoid production by the adrenal gland. In the Western world, Addison's disease is most commonly an autoimmune condition, in which the body produces antibodies against cells of the adrenal cortex.

Worldwide, the disease is more frequently caused by infection, especially from tuberculosis. A distinctive feature of Addison's disease is hyperpigmentation of the skin, which presents with other nonspecific symptoms such as fatigue. A complication seen in untreated Addison's disease and other types of primary adrenal insufficiency is the adrenal crisis , a medical emergency in which low glucocorticoid and mineralocorticoid levels result in hypovolemic shock and symptoms such as vomiting and fever. An adrenal crisis can progressively lead to stupor and coma.

In secondary adrenal insufficiency, a dysfunction of the hypothalamic-pituitary-adrenal axis leads to decreased stimulation of the adrenal cortex. Apart from suppression of the axis by glucocorticoid therapy, the most common cause of secondary adrenal insufficiency are tumors that affect the production of adrenocorticotropic hormone ACTH by the pituitary gland. Congenital adrenal hyperplasia is a congenital disease in which mutations of enzymes that produce steroid hormones result in a glucocorticoid deficiency and malfunction of the negative feedback loop of the HPA axis.

As cortisol cannot be synthesized, these hormones are released in high quantities and stimulate production of other adrenal steroids instead. The most common form of congenital adrenal hyperplasia is due to hydroxylase deficiency. Therefore, ACTH stimulation of the adrenal cortex induces the release of excessive amounts of adrenal androgens , which can lead to the development of ambiguous genitalia and secondary sex characteristics. Adrenal tumors are commonly found as incidentalomas , unexpected asymptomatic tumors found during medical imaging.

They are seen in around 3. Pheochromocytomas are tumors of the adrenal medulla that arise from chromaffin cells. They can produce a variety of nonspecific symptoms, which include headaches, sweating, anxiety and palpitations. Common signs include hypertension and tachycardia. Surgery, especially adrenal laparoscopy , is the most common treatment for small pheochromocytomas. Bartolomeo Eustachi , an Italian anatomist,is credited with the first description of the adrenal glands in The adrenal glands are named for their location relative to the kidneys.

The term "adrenal" comes from ad- Latin, "near" and renes Latin, "kidney". The suprarenal nature of the glands was not truly accepted until the 19th century, as anatomists clarified the ductless nature of the glands and their likely secretory role — prior to this, there was some debate as to whether the glands were indeed suprarenal or part of the kidney.

One of the most recognized works on the adrenal glands came in with the publication of On the Constitutional and Local Effects of Disease of the Suprarenal Capsule , by the English physician Thomas Addison. In his monography, Addison described what the French physician George Trousseau would later name Addison's disease , an eponym still used today for a condition of adrenal insufficiency and its related clinical manifestations. In the following decades several physicians experimented with extracts from the adrenal cortex to treat Addison's disease.

From Wikipedia, the free encyclopedia. Adrenal gland The adrenal glands lie above the kidneys. From Pathophysiology to Clinical Evidence. Retrieved 11 February A Text and Atlas 6th ed. Williams Textbook of Endocrinology 12th ed.

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