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Details for anatomical structure: cell of adrenal gland zona glomerulosa

EndoNet ID: ENC00168

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Synonyms

cell of adrenal gland zona glomerulosa, , Endocrinocytus corticalis

General information

secreting mineralocorticoids (principally aldosterone)

Links to other resources

Cytomer cy0011218

Larger structures

  • adrenal_cortex
  • adrenal_gland

Substructures

    Secreted hormones

    • Hormone: aldosterone

      • The principal regulators of aldosterone synthesis and secretion of aldosterone are angiotensin II, the concentration of extracellular potassium and ACTH. [1]
      • Classically, aldosterone is synthesised in the adrenal zona glomerulosa and binds to specific mineralocorticoid receptors located in the cytosol of target epithelial cells. [1]

      Influenced by:

      • CCK-2
        in cell_of_adrenal_gland_zona_glomerulosa
        • CCK stimulates aldosterone secretion via specific receptors (CCK1-Rs and CCK2-Rs in rats, and CCK2-Rs in humans) located in zona glomerulosa cells and coupled to the adenylate cyclase-dependent signaling cascade. [2]
        • CCK and the CCK2-R agonist pentagastrin enhanced basal aldosterone secretion from zona glomerulosa (ZG) cells without affecting cortisol production from zona fasciculata-reticularis cells. [3]
        • The aldosterone response to CCK and pentagastrin was suppressed by a CCK2-R antagonist, but not by a CCK1-R antagonist. [3]
        • In contrast with rats, in humans the aldosterone secretagogue effect of CCK appears to be exclusively mediated by CCK2-R. [3]
      • ACTH receptor
        in cell_of_adrenal_gland_zona_glomerulosa
        • The dopamine agonist cabergoline induced a significant stimulation at low dose and a significant inhibition at high dose of baseline and ACTH-stimulated aldosterone secretion. [4]
        • Acutely, ACTH stimulates aldosterone production via cAMP-mediated pathways and protein-synthesisindependent mechanisms involving macrophage-derived factor, steroidogenesis-inducing protein and calmidazolium. [1]
        • In contrast, chronic excess of ACTH suppresses plasma aldosterone levels in both humans and animal models. The mechanism of chronic inhibition is unclear but cAMP may downregulate the expression of Ang II receptors in adrenocortical cells. Alternatively, ACTH may transform proliferating ZG cells into zona fasciculata cells or divert precursors from the mineralocorticoid to the glucocorticoid pathway. [1]
      • 5-hydroxytryptamine receptor 4
        in cell_of_adrenal_gland_zona_glomerulosa
        • Released by mast cells in the vicinity of glomerulosa cells, 5-HT stimulates aldosterone secretion through activation of 5-HT4 receptors positively coupled to adenylyl cyclase and calcium influx. [5]
      • angiotensin II type 1 receptor
        in cell_of_adrenal_gland_zona_glomerulosa
        • Ang II acts on the adrenal zona glomerulosa to stimulate aldosterone production via specific G-protein-coupled receptors (AT1 receptors). [1]
        • The dopamine agonists bromocriptine and cabergoline induced a significant inhibition of the angiotensin II-induced aldosterone secretion, cabergoline being significantly more effective than bromocriptine. [4]
        • In vitro studies with isolated adrenal glomerulosa cells demonstrated that the activation of D2 receptors resulted in a remarkable inhibition of angiotensin II-induced aldosterone secretion, whereas it did not influence basal and ACTH induced aldosterone secretion. [4]
        • High concentration of alpha-MSH significantly inhibited Ang II-stimulated aldosterone secretion. [6]
      • Sphingosine 1-phosphate receptor 2
        in adrenal_gland
        • S1P is a novel regulator of aldosterone secretion, which is crucial for hemodynamic stability. The stimulation of aldosterone secretion by S1P involves the PLD/PAP pathway and that Gi proteins, extracellular Ca2+, and the PKC isoforms alpha and delta are all important components of the signaling pathways controlling this process. [7]
      • BMP receptor type II
        in adrenal_cortex
        • 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. [8]
        • Potassium-induced aldosterone production was not found to be influenced by BMP-6. [9]
      • BMP receptor type II
        in adrenal_cortex
        • Specifically, secretion of aldosterone, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [10]
        • 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. [10]
      • NPR1
        in adrenal_cortex
        • 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. [11]
        • ANP-dependent decreases in aldosterone secretion from the adrenal gland require reductions in cAMP concentrations. [12]
        • ANP-dependent activation of NPR-A produces cGMP and stimulates cAMP-hydrolyzing PDE2. [12]
      • dopamine receptor D2
        in cell_of_adrenal_gland_zona_glomerulosa
        • Dopmaine has an inhibitory effect on aldosterone secretion. Type 2 dopamine receptor has been demonstrated in the adrenal glomerulosa. [11]
      • dopamine receptor D1
        in cell_of_adrenal_gland_zona_glomerulosa
        • Dopmaine has an inhibitory effect on aldosterone secretion. Type 1 dopamine receptor has been demonstrated in the adrenal glomerulosa. [11]
      • VPAC2
        in cell_of_adrenal_gland_zona_glomerulosa
        • VIP and PACAP, acting via VPAC1 coupled to adenylate cyclase- and phospholipase C-dependent cascades, stimulate aldosterone secretion from zona glomerulosa cells. [13]
      • VPAC1
        in cell_of_adrenal_gland_zona_glomerulosa
        • VIP and PACAP, acting via VPAC1 coupled to adenylate cyclase- and phospholipase C-dependent cascades, stimulate aldosterone secretion from zona glomerulosa cells. [13]
      • CCK-1
        in cell_of_adrenal_gland_zona_glomerulosa
        • Rat adrenal zona glomerulosa expresses CCK1-R and CCK2-R and is provided with CCK-binding sites, whose activation enhances aldosterone secretion. Cholecystokinin, acting through these cholecystokinin receptors 1 and 2 coupled with the adenylate cyclase/PKA cascade, exerts a sizeable secretagogue action on rat zona glomerulosa cells. [14]
      • QRFP-R
        in cell_of_adrenal_gland_zona_glomerulosa
        • Considered together with the expression of QRFP-R mRNA in the adrenal gland, these results indicate that QRFP acts directly on the zona glomerulosa to induce aldosterone secretion in rats. [15]

    • Hormone: progesterone

      Influenced by:

      • LHCGR-1
        in cell_of_adrenal_gland_zona_glomerulosa
      • follitropin receptor
        in cell_of_adrenal_gland_zona_glomerulosa

    Receptors

    • Receptor: follitropin receptor

      Influences:

      • progesterone

    • Receptor: LHCGR-1

      Influences:

      • progesterone

    • Receptor: ACTH receptor

      Influences:

      • aldosterone
        • The dopamine agonist cabergoline induced a significant stimulation at low dose and a significant inhibition at high dose of baseline and ACTH-stimulated aldosterone secretion. [4]
        • Acutely, ACTH stimulates aldosterone production via cAMP-mediated pathways and protein-synthesisindependent mechanisms involving macrophage-derived factor, steroidogenesis-inducing protein and calmidazolium. [1]
        • In contrast, chronic excess of ACTH suppresses plasma aldosterone levels in both humans and animal models. The mechanism of chronic inhibition is unclear but cAMP may downregulate the expression of Ang II receptors in adrenocortical cells. Alternatively, ACTH may transform proliferating ZG cells into zona fasciculata cells or divert precursors from the mineralocorticoid to the glucocorticoid pathway. [1]

    • Receptor: IL-6R

    • Receptor: CCK-2

      Influences:

      • aldosterone
        • CCK stimulates aldosterone secretion via specific receptors (CCK1-Rs and CCK2-Rs in rats, and CCK2-Rs in humans) located in zona glomerulosa cells and coupled to the adenylate cyclase-dependent signaling cascade. [2]
        • CCK and the CCK2-R agonist pentagastrin enhanced basal aldosterone secretion from zona glomerulosa (ZG) cells without affecting cortisol production from zona fasciculata-reticularis cells. [3]
        • The aldosterone response to CCK and pentagastrin was suppressed by a CCK2-R antagonist, but not by a CCK1-R antagonist. [3]
        • In contrast with rats, in humans the aldosterone secretagogue effect of CCK appears to be exclusively mediated by CCK2-R. [3]

    • Receptor: angiotensin II type 1 receptor

      Induced phenotype:

      • positive regulation of phospholipid catabolic process
        • A number of cellular events are triggered by the interaction of AII with its receptor. These include phospholipid breakdown, with consequent increases in diacylglycerol, inositol phosphates and intracellular calcium, protein kinase C activation, inhibition of adenylate cyclase and arachidonic acid metabolism. [16]

      Influences:

      • aldosterone
        • Ang II acts on the adrenal zona glomerulosa to stimulate aldosterone production via specific G-protein-coupled receptors (AT1 receptors). [1]
        • The dopamine agonists bromocriptine and cabergoline induced a significant inhibition of the angiotensin II-induced aldosterone secretion, cabergoline being significantly more effective than bromocriptine. [4]
        • In vitro studies with isolated adrenal glomerulosa cells demonstrated that the activation of D2 receptors resulted in a remarkable inhibition of angiotensin II-induced aldosterone secretion, whereas it did not influence basal and ACTH induced aldosterone secretion. [4]
        • High concentration of alpha-MSH significantly inhibited Ang II-stimulated aldosterone secretion. [6]

    • Receptor: CCK-1

      Influences:

      • aldosterone
        • Rat adrenal zona glomerulosa expresses CCK1-R and CCK2-R and is provided with CCK-binding sites, whose activation enhances aldosterone secretion. Cholecystokinin, acting through these cholecystokinin receptors 1 and 2 coupled with the adenylate cyclase/PKA cascade, exerts a sizeable secretagogue action on rat zona glomerulosa cells. [14]

    • Receptor: dopamine receptor D2

      Influences:

      • aldosterone
        • Dopmaine has an inhibitory effect on aldosterone secretion. Type 2 dopamine receptor has been demonstrated in the adrenal glomerulosa. [11]

    • Receptor: dopamine receptor D4

    • Receptor: 5-hydroxytryptamine receptor 4

      Influences:

      • aldosterone
        • Released by mast cells in the vicinity of glomerulosa cells, 5-HT stimulates aldosterone secretion through activation of 5-HT4 receptors positively coupled to adenylyl cyclase and calcium influx. [5]

    • Receptor: dopamine receptor D1

      Influences:

      • aldosterone
        • Dopmaine has an inhibitory effect on aldosterone secretion. Type 1 dopamine receptor has been demonstrated in the adrenal glomerulosa. [11]

    • Receptor: VPAC2

      Influences:

      • aldosterone
        • VIP and PACAP, acting via VPAC1 coupled to adenylate cyclase- and phospholipase C-dependent cascades, stimulate aldosterone secretion from zona glomerulosa cells. [13]

    • Receptor: VPAC1

      Influences:

      • aldosterone
        • VIP and PACAP, acting via VPAC1 coupled to adenylate cyclase- and phospholipase C-dependent cascades, stimulate aldosterone secretion from zona glomerulosa cells. [13]

    • Receptor: QRFP-R

      • A high level of QFRP-R mRNA expression was detected in the zona glomerulosa of the adrenal gland. [15]

      Influences:

      • aldosterone
        • Considered together with the expression of QRFP-R mRNA in the adrenal gland, these results indicate that QRFP acts directly on the zona glomerulosa to induce aldosterone secretion in rats. [15]
    Reference