Adrenal cortex

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Adrenal cortex
Gray1185.png
Layers of cortex.
Adrenal cortex labelled.jpg
The adrenal cortex
Details
Precursor mesoderm [1]
Identifiers
Latin cortex glandulae suprarenalis
MeSH D000302
TA98 A11.5.00.007
A13.2.03.005
TA2 3881
FMA 15632
Anatomical terminology

The adrenal cortex is the outer region and also the largest part of the adrenal gland. It is divided into three separate zones: zona glomerulosa, zona fasciculata and zona reticularis. Each zone is responsible for producing specific hormones. It is also a secondary site of androgen synthesis. [2]

Contents

Layers

The adrenal cortex comprises three main zones, or layers that are regulated by distinct hormones as noted below. This anatomic zonation can be appreciated at the microscopic level, where each zone can be recognized and distinguished from one another based on structural and anatomic characteristics. [3]

Zona glomerulosa

The outermost layer, the zona glomerulosa is the main site for the production of aldosterone, a mineralocorticoid. The synthesis and secretion of aldosterone are mainly regulated by the renin–angiotensin–aldosterone system. The zona glomerulosa cells express a specific enzyme aldosterone synthase (also known as CYP11B2). [4] [5] Aldosterone is largely responsible for the long-term regulation of blood pressure. [6] Aldosterone's effects are on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). [6] Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation. Although sustained production of aldosterone requires persistent calcium entry through low-voltage activated Ca2+ channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca2+ channels entry. [7]

The secretion of aldosterone is also stimulated by adrenocorticotropic hormone (ACTH). [8]

The cells of the zona glomerulosa do not express 11β-hydroxylase and 17α-hydroxylase. This is the reason zona glomerulosa cannot synthesize cortisol, corticosterone or sex hormones (androgens). [9] The expression of neuron-specific proteins in the zona glomerulosa cells of human adrenocortical tissues has been predicted and reported by several authors [10] [11] [12] and it was suggested that the expression of proteins like the neuronal cell adhesion molecule (NCAM) in the cells of the zona glomerulosa reflects the regenerative feature of these cells, which would lose NCAM immunoreactivity after moving to the zona fasciculata. [10] [13] However, together with other data on neuroendocrine properties of zona glomerulosa cells, NCAM expression may reflect a neuroendocrine differentiation of these cells. [10]

Zona fasciculata

Situated between the glomerulosa and reticularis, the cells of the zona fasciculata synthesize and secrete glucocorticoids (such as 11-deoxycorticosterone, corticosterone, and cortisol), as well as small amounts of adrenal androgens and estrogens. [14] The zona fasciculata has more 3β-hydroxysteroid dehydrogenase activity than the zona reticularis. Therefore, the zona fasciculata makes more 11-deoxycorticosterone, corticosterone, and cortisol. [9] The major hormone that stimulates cortisol secretion in humans is the ACTH that is released from the anterior pituitary. [8] It has been shown that the steroidogenic capacity of the zona fasciculata increases during illness in infants. [8]

Zona reticularis

The inner most cortical layer, the zona reticularis produces adrenal androgens, as well as small amounts of estrogens and some glucocorticoids. [14] The zona reticularis has more of the cofactors required for the 17,20-lyase activity of 17α-hydroxylase than zona fasciculata. Therefore, the zona reticularis makes more androgens, [9] mainly dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (the precursor to testosterone) in humans. The secretion of DHEAS is also stimulated by ACTH. [8]

Hormone synthesis

Adrenal steroid pathways Adrenal Steroids Pathways - edited.svg
Adrenal steroid pathways

The precursor of steroids synthesized in the adrenal cortex is cholesterol that is stored in vesicles. Cholesterol can be synthesized de novo in the adrenal cortex. Yet, the major source of cholesterol appears to be cholesterol that is taken up with circulating lipoproteins. [15]

The steps up to this point occur in many steroid-producing tissues. Subsequent steps to generate aldosterone and cortisol, however, primarily occur in the adrenal cortex:

Adrenal steroid hormone synthesis steps Adrenal steroid hormone synthesis.png
Adrenal steroid hormone synthesis steps

Production

The adrenal cortex produces a number of different corticosteroid hormones.

Mineralocorticoids

The primary mineralocorticoid, aldosterone, is produced in the adrenocortical zona glomerulosa by the action of the enzyme aldosterone synthase (also known as CYP11B2). [4] [5] Aldosterone is largely responsible for the long-term regulation of blood pressure. [6] Aldosterone effects on the distal convoluted tubule and collecting duct of the kidney where it causes increased reabsorption of sodium and increased excretion of both potassium (by principal cells) and hydrogen ions (by intercalated cells of the collecting duct). [6] Sodium retention is also a response of the distal colon, and sweat glands to aldosterone receptor stimulation. Although sustained production of aldosterone requires persistent calcium entry through low-voltage activated Ca2+ channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca2+ channels entry. [7]

Glucocorticoids

Glucocorticoids are produced mainly in the zona fasciculata. [9] The primary glucocorticoid released by the adrenal gland is cortisol in humans and corticosterone in many other animals. Its secretion is regulated by the hormone ACTH from the anterior pituitary.[ citation needed ]

Androgens

They are produced mainly in the zona reticularis. [9] The most important androgens include:

Pathology

See also

Related Research Articles

<span class="mw-page-title-main">Adrenal gland</span> Endocrine gland

The adrenal glands are endocrine glands that produce a variety of hormones including adrenaline and the steroids aldosterone and cortisol. They are found above the kidneys. Each gland has an outer cortex which produces steroid hormones and an inner medulla. The adrenal cortex itself is divided into three main zones: the zona glomerulosa, the zona fasciculata and the zona reticularis.

<span class="mw-page-title-main">Adrenocorticotropic hormone</span> Pituitary hormone

Adrenocorticotropic hormone is a polypeptide tropic hormone produced by and secreted by the anterior pituitary gland. It is also used as a medication and diagnostic agent. ACTH is an important component of the hypothalamic-pituitary-adrenal axis and is often produced in response to biological stress. Its principal effects are increased production and release of cortisol and androgens by the cortex and medulla of the adrenal gland, respectively. ACTH is also related to the circadian rhythm in many organisms.

<span class="mw-page-title-main">Cortisol</span> Human natural glucocorticoid hormone

Cortisol is a steroid hormone, in the glucocorticoid class of hormones and a stress hormone. When used as a medication, it is known as hydrocortisone.

<span class="mw-page-title-main">Aldosterone</span> Mineralocorticoid steroid hormone

Aldosterone is the main mineralocorticoid steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands, and colon. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium (Na+), and potassium (K+) levels. It does so primarily by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It influences the reabsorption of sodium and excretion of potassium (from and into the tubular fluids, respectively) of the kidney, thereby indirectly influencing water retention or loss, blood pressure, and blood volume. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and kidney disease. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart.

<span class="mw-page-title-main">Corticosterone</span> Chemical compound

Corticosterone, also known as 17-deoxycortisol and 11β,21-dihydroxyprogesterone, is a 21-carbon steroid hormone of the corticosteroid type produced in the cortex of the adrenal glands. In the very rare case of congenital adrenal hyperplasia due to 17α-hydroxylase deficiency cortisol production is blocked.

<span class="mw-page-title-main">Mineralocorticoid</span> Group of corticosteroids

Mineralocorticoids are a class of corticosteroids, which in turn are a class of steroid hormones. Mineralocorticoids are produced in the adrenal cortex and influence salt and water balances. The primary mineralocorticoid is aldosterone.

<span class="mw-page-title-main">Adrenal insufficiency</span> Medical condition

Adrenal insufficiency is a condition in which the adrenal glands do not produce adequate amounts of steroid hormones. The adrenal glands—also referred to as the adrenal cortex—normally secrete glucocorticoids, mineralocorticoids, and androgens. These hormones are important in regulating blood pressure, electrolytes, and metabolism as a whole. Deficiency of these hormones leads to symptoms ranging from abdominal pain, vomiting, muscle weakness and fatigue, low blood pressure, depression, mood and personality changes to organ failure and shock. Adrenal crisis may occur if a person having adrenal insufficiency experiences stresses, such as an accident, injury, surgery, or severe infection; this is a life-threatening medical condition resulting from severe deficiency of cortisol in the body. Death may quickly follow.

<span class="mw-page-title-main">Lipoid congenital adrenal hyperplasia</span> Medical condition

Lipoid congenital adrenal hyperplasia is an endocrine disorder that is an uncommon and potentially lethal form of congenital adrenal hyperplasia (CAH). It arises from defects in the earliest stages of steroid hormone synthesis: the transport of cholesterol into the mitochondria and the conversion of cholesterol to pregnenolone—the first step in the synthesis of all steroid hormones. Lipoid CAH causes mineralocorticoid deficiency in affected infants and children. Male infants are severely undervirilized causing their external genitalia to look feminine. The adrenals are large and filled with lipid globules derived from cholesterol.

Congenital adrenal hyperplasia due to 17α-hydroxylase deficiency is an uncommon form of congenital adrenal hyperplasia resulting from a defect in the gene CYP17A1, which encodes for the enzyme 17α-hydroxylase. It causes decreased synthesis of cortisol and sex steroids, with resulting increase in mineralocorticoid production. Thus, common symptoms include mild hypocortisolism, ambiguous genitalia in genetic males or failure of the ovaries to function at puberty in genetic females, and hypokalemic hypertension (respectively). However, partial (incomplete) deficiency is notable for having inconsistent symptoms between patients, and affected genetic (XX) females may be wholly asymptomatic except for infertility.

<span class="mw-page-title-main">Zona reticularis</span> Layer of adrenal cortex

The zona reticularis is the innermost layer of the adrenal cortex, lying deep to the zona fasciculata and superficial to the adrenal medulla. The cells are arranged cords that project in different directions giving a net-like appearance.

<span class="mw-page-title-main">Zona glomerulosa</span> Part of the adrenal gland

The zona glomerulosa of the adrenal gland is the most superficial layer of the adrenal cortex, lying directly beneath the renal capsule. Its cells are ovoid and arranged in clusters or arches.

<span class="mw-page-title-main">Zona fasciculata</span>

The zona fasciculata constitutes the middle and also the widest zone of the adrenal cortex, sitting directly beneath the zona glomerulosa. Constituent cells are organized into bundles or "fascicles".

In humans and other animals, the adrenocortical hormones are hormones produced by the adrenal cortex, the outer region of the adrenal gland. These polycyclic steroid hormones have a variety of roles that are crucial for the body’s response to stress, and they also regulate other functions in the body. Threats to homeostasis, such as injury, chemical imbalances, infection, or psychological stress, can initiate a stress response. Examples of adrenocortical hormones that are involved in the stress response are aldosterone and cortisol. These hormones also function in regulating the conservation of water by the kidneys and glucose metabolism, respectively.

<span class="mw-page-title-main">11-Deoxycorticosterone</span> Chemical compound

11-Deoxycorticosterone (DOC), or simply deoxycorticosterone, also known as 21-hydroxyprogesterone, as well as desoxycortone (INN), deoxycortone, and cortexone, is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. It is an active (Na+-retaining) mineralocorticoid. As its names indicate, 11-deoxycorticosterone can be understood as the 21-hydroxy-variant of progesterone or as the 11-deoxy-variant of corticosterone.

<span class="mw-page-title-main">Aldosterone synthase</span> Protein-coding gene in the species Homo sapiens

Aldosterone synthase, also called steroid 18-hydroxylase, corticosterone 18-monooxygenase or P450C18, is a steroid hydroxylase cytochrome P450 enzyme involved in the biosynthesis of the mineralocorticoid aldosterone and other steroids. The enzyme catalyzes sequential hydroxylations of the steroid angular methyl group at C18 after initial 11β-hydroxylation. It is encoded by the CYP11B2 gene in humans.

<span class="mw-page-title-main">Steroid 11β-hydroxylase</span> Protein found in mammals

Steroid 11β-hydroxylase, also known as steroid 11β-monooxygenase, is a steroid hydroxylase found in the zona glomerulosa and zona fasciculata of the adrenal cortex. Named officially the cytochrome P450 11B1, mitochondrial, it is a protein that in humans is encoded by the CYP11B1 gene. The enzyme is involved in the biosynthesis of adrenal corticosteroids by catalyzing the addition of hydroxyl groups during oxidation reactions.

<span class="mw-page-title-main">Adrenocortical adenoma</span> Medical condition

An adrenocortical adenoma or adrenal adenoma is commonly described as a benign neoplasm emerging from the cells that comprise the adrenal cortex. Like most adenomas, the adrenocortical adenoma is considered a benign tumor since the majority of them are non-functioning and asymptomatic. Adrenocortical adenomas are classified as ACTH-independent disorders, and are commonly associated with conditions linked to hyperadrenalism such as Cushing's syndrome (hypercortisolism) or Conn's syndrome (hyperaldosteronism), which is also known as primary aldosteronism. In addition, recent case reports further support the affiliation of adrenocortical adenomas with hyperandrogenism or florid hyperandrogenism which can cause hyperandrogenic hirsutism in females. "Cushing's syndrome" differs from the "Cushing's disease" even though both conditions are induced by hypercortisolism. The term "Cushing's disease" refers specifically to "secondary hypercortisolism" classified as "ACTH-dependent Cushing's syndrome" caused by pituitary adenomas. In contrast, "Cushing's syndrome" refers specifically to "primary hypercortisolism" classified as "ACTH-independent Cushing's syndrome" caused by adrenocortical adenomas.

The ACTH test is a medical test usually requested and interpreted by endocrinologists to assess the functioning of the adrenal glands' stress response by measuring the adrenal response to adrenocorticotropic hormone or another corticotropic agent such as tetracosactide or alsactide (Synchrodyn). ACTH is a hormone produced in the anterior pituitary gland that stimulates the adrenal glands to release cortisol, dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and aldosterone.

Glucocorticoid remediable aldosteronism also describable as aldosterone synthase hyperactivity, is an autosomal dominant disorder in which the increase in aldosterone secretion produced by ACTH is no longer transient.

Adrenal steroids are steroids that are derived from the adrenal glands. They include corticosteroids, which consist of glucocorticoids like cortisol and mineralocorticoids like aldosterone, adrenal androgens like dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (A4), and neurosteroids like DHEA and DHEA-S, as well as pregnenolone and pregnenolone sulfate (P5-S). Adrenal steroids are specifically produced in the adrenal cortex.

References

  1. ↑ "Embryology of the adrenal gland" . Retrieved 2007-12-11.
  2. ↑ Anatomy Atlases – Microscopic Anatomy, plate 15.292 – "Adrenal Gland"
  3. ↑ Whitehead, Saffron A.; Nussey, Stephen (2001). Endocrinology: an integrated approach. Oxford: BIOS. p. 122. ISBN   978-1-85996-252-7.
  4. 1 2 Curnow KM, Tusie-Luna MT, Pascoe L, et al. (October 1991). "The product of the CYP11B2 gene is required for aldosterone biosynthesis in the human adrenal cortex". Mol. Endocrinol. 5 (10): 1513–22. doi: 10.1210/mend-5-10-1513 . PMID   1775135.
  5. 1 2 Zhou M, Gomez-Sanchez CE (July 1993). "Cloning and expression of a rat cytochrome P-450 11 beta-hydroxylase/aldosterone synthase (CYP11B2) cDNA variant". Biochem. Biophys. Res. Commun. 194 (1): 112–7. doi:10.1006/bbrc.1993.1792. PMID   8333830.
  6. 1 2 3 4 Marieb Human Anatomy & Physiology 9th edition, chapter:16, page:629, question number:14
  7. 1 2 Hu C, Rusin CG, Tan Z, Guagliardo NA, Barrett PQ (June 2012). "Zona glomerulosa cells of the mouse adrenal cortex are intrinsic electrical oscillators". J. Clin. Invest. 122 (6): 2046–53. doi:10.1172/JCI61996. PMC   3966877 . PMID   22546854.
  8. 1 2 3 4 Hanukoglu A, Fried D, Nakash I, Hanukoglu I (Nov 1995). "Selective increases in adrenal steroidogenic capacity during acute respiratory disease in infants". Eur J Endocrinol. 133 (5): 552–6. doi:10.1530/eje.0.1330552. PMID   7581984. S2CID   44439040.
  9. 1 2 3 4 5 Barrett, Kim E. (2019). Ganong's review of medical physiology. Susan M. Barman, Heddwen L. Brooks, Jason X.-J. Yuan, William F. Preceded by: Ganong (26th ed.). [New York]. p. 337. ISBN   9781260122404. OCLC   1076268769.{{cite book}}: CS1 maint: location missing publisher (link)
  10. 1 2 3 Ehrhart-Bornstein M, Hilbers U (1998). "Neuroendocrine properties of adrenocortical cells". Horm. Metab. Res. 30 (6–7): 436–9. doi:10.1055/s-2007-978911. PMID   9694576. S2CID   260169208.
  11. ↑ Lefebvre H, Cartier D, Duparc C, et al. (March 2002). "Characterization of serotonin(4) receptors in adrenocortical aldosterone-producing adenomas: in vivo and in vitro studies". J. Clin. Endocrinol. Metab. 87 (3): 1211–6. doi:10.1210/jcem.87.3.8327. PMID   11889190.
  12. ↑ Ye P, Mariniello B, Mantero F, Shibata H, Rainey WE (October 2007). "G-protein-coupled receptors in aldosterone-producing adenomas: a potential cause of hyperaldosteronism". J. Endocrinol. 195 (1): 39–48. doi: 10.1677/JOE-07-0037 . PMID   17911395.
  13. ↑ Haidan A, Bornstein SR, Glasow A, Uhlmann K, Lübke C, Ehrhart-Bornstein M (February 1998). "Basal steroidogenic activity of adrenocortical cells is increased 10-fold by coculture with chromaffin cells". Endocrinology. 139 (2): 772–80. doi: 10.1210/endo.139.2.5740 . PMID   9449652.
  14. 1 2 Hall, John E. (2021). Guyton and Hall textbook of medical physiology. Michael E. Hall (14th ed.). Philadelphia, PA. p. 956. ISBN   978-0-323-59712-8. OCLC   1129099861.{{cite book}}: CS1 maint: location missing publisher (link)
  15. ↑ London E, Wassif CA, Horvath A, Tatsi C, Angelousi A, Karageorgiadis AS, Porter FD, Stratakis CA (2015). "Cholesterol Biosynthesis and Trafficking in Cortisol-Producing Lesions of the Adrenal Cortex". J Clin Endocrinol Metab. 100 (10): 3660–7. doi:10.1210/jc.2015-2212. PMC   4596036 . PMID   26204136.
  16. ↑ Rainey WE, Nakamura Y (February 2008). "Regulation of the adrenal androgen biosynthesis". J. Steroid Biochem. Mol. Biol. 108 (3–5): 281–6. doi:10.1016/j.jsbmb.2007.09.015. PMC   2699571 . PMID   17945481.
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