副腎皮質の、副腎皮質性の

関: adrenal cortex、adrenal cortical、adrenal cortices

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of or derived from the cortex of the adrenal glands

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/08/17 08:04:02」(JST)

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Hematoxylin-eosin staining of a non-pathological adrenal gland. The pointer shows the adrenal cortex

Situated along the perimeter of the adrenal gland, the adrenal cortex mediates the stress response through the production of mineralocorticoids and glucocorticoids, including aldosterone and cortisol respectively. It is also a secondary site of androgen synthesis.^[2] Recent data suggest that adrenocortical cells under pathological as well as under physiological conditions show neuroendocrine properties; within the normal adrenal, this neuroendocrine differentiation seems to be restricted to cells of the zona glomerulosa and might be important for an autocrine regulation of adrenocortical function.^[3]

Layers

The adrenal cortex comprises nine zones, or layers. 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.^[4] The adrenal cortex exhibits functional zonation as well: by virtue of the characteristic enzymes present in each zone, the zones produce and secrete distinct hormones.^[4]

Zona glomerulosa: The outermost layer, the zona glomerulosa is the main site for production of aldosterone, a mineralocorticoid, by the action of the enzyme aldosterone synthase (also known as CYP11B2).^[5]^[6] Aldosterone is largely responsible for the long-term regulation of blood pressure.^[7] 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).^[7] 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.^[8] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca²⁺ channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production.^[8] Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the juxtaglomerular cells of the kidney.^[9]

Paraffin sections of human adrenals immunostained for neuronal cell adhesion molecule (NCAM). Immunohistochemistry was carried out using 4-amino-9-ethylcarbazole(AEC; Dinanova, Hamburg, Germany) and were counterstained with hematoxylin. Staining for NCAM was restricted to the zona glomerulosa (zg) and the adrenal medulla (m); a: x 20; b: x 200.^[3]

The expression of neuron-specific proteins in the zona glomerulosa cells of human adrenocortical tissues has been predicted and reported by several authors^[3]^[10]^[11] 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.^[3]^[12] However, together with other data on neuroendocrine properties of zona glomerulosa cells, NCAM expression may reflect a neuroendocrine differentiation of these cells.^[3]

Zona fasciculata: Situated between the glomerulosa and reticularis, the zona fasciculata is responsible for producing glucocorticoids, such as 11-deoxycorticosterone, corticosterone, and cortisol in humans. Cortisol is the main glucocorticoid under normal conditions and its actions include mobilization of fats, proteins, and carbohydrates, but it does not increase under starvation conditions.^[9] Additionally, cortisol enhances the activity of other hormones including glucagon and catecholamines. The zona fasciculata secretes a basal level of cortisol but can also produce bursts of the hormone in response to adrenocorticotropic hormone (ACTH) from the anterior pituitary.

Zona reticularis: The inner most cortical layer, the zona reticularis produces androgens, mainly dehydroepiandrosterone (DHEA), DHEA sulfate (DHEA-S), and androstenedione (the precursor to testosterone) in humans.^[9]

Hormone synthesis

All adrenocortical steroid hormones are synthesized from cholesterol. Cholesterol is transported into the adrenal gland. 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:

Progesterone → (hydroxylation at C21) → 11-Deoxycorticosterone → (two further hydroxylations at C11 and C18) → Aldosterone
Progesterone → (hydroxylation at C17) → 17-alpha-hydroxyprogesterone → (hydroxylation at C21) → 11-Deoxycortisol → (hydroxylation at C11) → Cortisol

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).^[5]^[6] Aldosterone is largely responsible for the long-term regulation of blood pressure.^[7] 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).^[7] 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.^[8] However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca²⁺ channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production.^[8] Angiotensin II originates from plasmatic angiotensin I after the conversion of angiotensinogen by renin produced by the juxtaglomerular cells of the kidney.^[9]

Glucocorticoids

They are produced in the zona fasciculata. 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. Upon binding to its target, cortisol enhances metabolism in several ways:

It stimulates the release of amino acids from the body
It stimulates lipolysis, the breakdown of fat
It stimulates gluconeogenesis, the production of glucose from newly released amino acids and lipids
It increases blood glucose levels in response to stress, by inhibiting glucose uptake into muscle and fat cells
It strengthens cardiac muscle contractions
It increases water retention
It has anti-inflammatory and anti-allergic effects

Androgens

They are produced in the zona reticularis. The most important androgens include:

Testosterone: a hormone with a wide variety of effects, ranging from enhancing muscle mass and stimulation of cell growth to the development of the secondary sex characteristics.
Dihydrotestosterone (DHT): a metabolite of testosterone, and a more potent androgen than testosterone in that it binds more strongly to androgen receptors.
Androstenedione (Andro): an androgenic steroid produced by the testes, adrenal cortex, and ovaries. While androstenediones are converted metabolically to testosterone and other androgens, they are also the parent structure of estrone.
Dehydroepiandrosterone (DHEA): It is the primary precursor of natural estrogens. DHEA is also called dehydroisoandrosterone or dehydroandrosterone. The reticularis also produces DHEA-sulfate due to the actions of a sulfotransferase, SULT2A1.^[13]

Pathology

Adrenal insufficiency (e.g. due to Addison's disease)
Cushing's syndrome
Conn's syndrome
Adrenal Virilism

References

^ "Embryology of the adrenal gland". Retrieved 2007-12-11.
^ Anatomy Atlases - Microscopic Anatomy, plate 15.292 - "Adrenal Gland"
^ ^a ^b ^c ^d ^e 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.
^ ^a ^b Whitehead, Saffron A.; Nussey, Stephen (2001). Endocrinology: an integrated approach. Oxford: BIOS. p. 122. ISBN 1-85996-252-1.
^ ^a ^b 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.
^ ^a ^b 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.
^ ^a ^b ^c ^d Marieb Human Anatomy & Physiology 9th edition, chapter:16, page:629, question number:14
^ ^a ^b ^c ^d 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. PMID 22546854.
^ ^a ^b ^c ^d Dunn R. B.; Kudrath W.; Passo S.S.; Wilson L.B. (2011). "10". Kaplan USMLE Step 1 Physiology Lecture Notes. pp. 263–289.
^ 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/jc.87.3.1211. PMID 11889190.
^ 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.
^ 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/en.139.2.772. PMID 9449652.
^ 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.

External links

Anatomy photo:40:04-0203 at the SUNY Downstate Medical Center - "Posterior Abdominal Wall: Blood Supply to the Suprarenal Glands"
Mnemonic medicalmnemonics.com 180 2201 412
Histology image: 14502loa - Histology Learning System at Boston University
Adrenal Cortex Medical Notes on rahulgladwin.com

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リンク元	「副腎皮質性」「adrenal cortices」「adrenal cortical」
拡張検索	「iatrogenic adrenocortical insufficiency」「secondary adrenocortical insufficiency」「primary chronic adrenocortical insufficiency」「congenital adrenocortical hyperplasia」「chronic adrenocortical insufficiency」