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Details for anatomical structure: adrenal cortex

EndoNet ID: ENC00007

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Synonyms

adrenal cortex, cortex of suprarenal gland, suprarenal cortex, cortex of adrenal gland, Cortex glandulae suprarenalis

General information

The outer part of the adrenal gland, consisting of three zones from without inward: zona glomerulosa, zona fasciculata, and zona reticularis; this part of the adrenal cortex yields steroid hormones, such as corticosterone, deoxycorticosterone, and estrone

Links to other resources

Cytomer cy0000526

Larger structures

  • adrenal_gland

Substructures

  • cell_of_adrenal_gland_zona_reticularis
  • cell_of_adrenal_gland_zona_glomerulosa
  • cell_of_adrenal_gland_zona_fasciculata

Secreted hormones

  • Hormone: cortisol

    Influenced by:

    • VPAC1
      in adrenal_cortex
      • Vasoactive intestinal peptide (VIP) was shown in a dose-dependent manner to increase cortisol secretion in human adrenocortical carcinoma, coupled with a parallel increase in cAMP accumulation. Treatment with the VPAC1 receptor agonist, produced a dose-dependent increase in cortisol secretion similar to that seen with VIP. [1]
      • VIP directly stimulates cortisol secretion via activation of the VPAC1 receptor subtype. [1]
    • BMP receptor type II
      in adrenal_cortex
      • In contrast to BMP-6, it could be recently demonstrated that both BMP-2 and BMP-5 are able to overall suppress forskolin-induced steroidogenesis in NCIh295R cells. [2]
      • Specifically, secretion of cortisol, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [2]

  • Hormone: corticosterone

  • Hormone: deoxycorticosterone

  • Hormone: dehydro-3-epiandrosterone

  • Hormone: androstenedione

  • Hormone: DHT

    • DHT significantly reduces human adrenocortical cell growth in vitro. DHT-induced growth inhibition could be mediated at least in part by TGFb1. [3]

  • Hormone: testosterone

  • Hormone: TGF-beta 1

    • TGF-beta1 is an important regulator of human adrenal development. [3]
    • TGF-beta1 and its receptor (type II) are expressed in human adrenocortical cells. [3]
    • TGF-beta1 reduces the proliferation of the adrenocortical cancer cell line in vitro. [3]

    Influenced by:

    • AR
      in adrenal_cortex
      • In a human adrenocortical cell line, DHT is capable of up-regulating both TGF-beta1 mRNA and protein. [3]

  • Hormone: IL-18

  • Hormone: persephin

  • Hormone: BMP4

Receptors

  • Receptor: PRLR

    Induced phenotype:

    • positive regulation of steroid biosynthetic process
      • A direct action of PRL on adrenal steroidogenesis has been reported. Specifically, PRL is able to increase adrenal androgens, dihydroepiandrosterone and dihydroepianstrosterone sulfate as well as cortisol and aldosterone. [4]

  • Receptor: IGF-1R

  • Receptor: IGF-2R

  • Receptor: FGFR-2

  • Receptor: AR

    Influences:

    • TGF-beta 1
      • In a human adrenocortical cell line, DHT is capable of up-regulating both TGF-beta1 mRNA and protein. [3]

  • Receptor: TGF-beta type II receptor

  • Receptor: GRP-R

  • Receptor: LRP5

  • Receptor: VPAC1

    Influences:

    • cortisol
      • Vasoactive intestinal peptide (VIP) was shown in a dose-dependent manner to increase cortisol secretion in human adrenocortical carcinoma, coupled with a parallel increase in cAMP accumulation. Treatment with the VPAC1 receptor agonist, produced a dose-dependent increase in cortisol secretion similar to that seen with VIP. [1]
      • VIP directly stimulates cortisol secretion via activation of the VPAC1 receptor subtype. [1]

  • Receptor: angiotensin II type 1 receptor

    Induced phenotype:

    • positive regulation of renal sodium ion absorption
      • In the adrenal cortex, their activation stimulates the release of aldosterone, thereby promoting sodium reabsorption in the mineralocorticoid-responsive segments of the distal nephron. [5]

  • Receptor: BMP receptor type II

    Induced phenotype:

    • negative regulation of steroid hormone biosynthetic
      • In contrast to BMP-6, it recently could be demonstrated that both BMP-2 and BMP-5 are able to overall suppress forskolin-induced steroidogenesis in NCIh295R cells. [2]
      • Specifically, secretion of aldosterone, cortisol, and dehydroepiandrosterone-sulphate, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [2]
    • regulation of steroid biosynthetic process
      • Endogenous BMP-6 produced by adrenocortical cells could play an important autocrine role in modulating the steroidogenic actions of Ang II. [6]
    • negative regulation of adrenocorticotropin receptor activity
      • Expression levels of several steroidogenic enzymes, catalyzing the different steps of hormone production, as well as the ACTH receptor (melanocortin 2 receptor), were also inhibited by BMP-2 and BMP-5 treatment in a dose- and time-dependent manner. [2]

    Influences:

    • aldosterone
      • In vitro experiments in NCIh295R adrenocortical tumour cells have revealed BMP-6-induced and SMAD1/SMAD5/SMAD8-mediated augmentation of aldosterone secretion through a crosstalk with Ang II-dependent pathways. [7]
      • Potassium-induced aldosterone production was not found to be influenced by BMP-6. [6]
    • aldosterone
      • Specifically, secretion of aldosterone, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [2]
      • In contrast to BMP-6, it could be recently demonstrated that both BMP-2 and BMP-5 are able to overall suppress forskolin-induced steroidogenesis in NCIh295R cells. [2]
    • cortisol
      • In contrast to BMP-6, it could be recently demonstrated that both BMP-2 and BMP-5 are able to overall suppress forskolin-induced steroidogenesis in NCIh295R cells. [2]
      • Specifically, secretion of cortisol, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [2]

  • Receptor: BMP receptor type 1A

    Induced phenotype:

    • Familial juvenile polyposis
      • Familial juvenile polyposis, an inherited hamartomatous polyposis syndrome with a high risk for colon cancer, has been associated with mutations in SMAD4 or BMPR1A. [8]

  • Receptor: NPR1

    Influences:

    • aldosterone
      • In humans and experimental animals, administration of atrial natriuretic peptide (ANP) decreases plasma aldosterone levels by direct inhibition of steroid biosynthesis at the adrenal level. [9]
      • ANP-dependent decreases in aldosterone secretion from the adrenal gland require reductions in cAMP concentrations. [10]
      • ANP-dependent activation of NPR-A produces cGMP and stimulates cAMP-hydrolyzing PDE2. [10]

  • Receptor: FGFR-1

  • Receptor: ACTH receptor

    Induced phenotype:

    • Cushing syndrome
    • Familial glucocorticoid deficiency type I
      • Mutations in the ACTH receptor (melanocortin 2 receptor) cause FGD types 1. [11]
    • Glucocorticoid remediable aldosteronism
      • GRA appears to be the most common monogenic form of human hypertension. As a result of chimeric gene duplication, aldosterone is ectopically synthesized in the zona fasciculata of the adrenal gland under the control of adrenocorticotropin (ACTH). [12]
    • Adrenocortical carcinoma
    • Addison disease
      • Congenital adrenal hypoplasia (AHC), mutations of steroidogenic factor-1, and ACTH unresponsiveness can all lead to adrenal dysgenesis/hypoplasia, albeit the latter usually results in isolated deficiency of glucocorticoids. [13]
Reference