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Details for messenger / hormone: aldosterone

EndoNet ID: ENH00005

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  • aldosterone
  • 11beta,21-Dihydroxy-3,20-dioxo-4-pregnen-18-al
  • aldo
  • Electrocortin
  • Aldocortin
  • 3,20-Diketo-11b,18-oxido-4-pregnene-18,21-diol

General information

  • Classically, aldosterone acts on epithelial cells, particularly in the renal collecting duct, but also in the parotid gland and colon, where it regulates the transport of Na+, K+ and water. [1]
  • In the vascular system, aldosterone is known to modulate vascular tone, possibly by increasing the pressor response to catecholamines and impairing the vasodilatory response to acetylcholine or by upregulation of Ang II receptor. [1]
  • Aldosterone escapes during long-term blockade of the renin-angiotensin-aldosterone system is associated with an enhanced decline in GFR in patients. [2]
  • Aldosterone plays a role in the initiation and progression of renal disease independently of arterial blood pressure and plasma angiotensin II levels. [2]
  • At the effective antihypertensive doses of efonidipine and amlodipine, efonidipine significantly decreases heart rate and plasma aldosterone level compared with those under amlodipine treatment in hypertensive patients. [3]
  • Aldosterone is synthesized from cholesterol in the zona glomerulosa (ZG) of the adrenal cortex. [1]
  • The increase of aldosterone excretion in subjects with resistant hypertension and symptoms of sleep apnea. [4]
  • Eplerenone, a new selective aldosterone blocker, was as effective as amlodipine in the treatment of older hypertensive patients with systolic hypertension, characterized by a widened pulse pressure. [5]
  • Ratio of serum aldosterone to plasma renin concentration in essential hypertension and primary aldosteronism. [6]
  • Endothelial cell signals modulate aldosterone release from the zone glomerulosa cells. [7]


Hormone function

  • homeostasis
    • cardiovascular control
      • ion flow control

      Chemical classification

      • hormone
        • not genome-encoded
          • sterol lipids
            • steroids
              • mineralcorticoids


        KEGG C01780

        Links to other resources

        KEGG C01780
        LIPID MAPS LMST02030026
        LipidBank SST0129
        • Anatomical structure: cell_of_adrenal_gland_zona_glomerulosa

          • 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. [8]
            • 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. [9]
            • The aldosterone response to CCK and pentagastrin was suppressed by a CCK2-R antagonist, but not by a CCK1-R antagonist. [9]
            • In contrast with rats, in humans the aldosterone secretagogue effect of CCK appears to be exclusively mediated by CCK2-R. [9]
          • 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. [10]
            • 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. [11]
          • 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. [10]
            • 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. [10]
            • High concentration of alpha-MSH significantly inhibited Ang II-stimulated aldosterone secretion. [12]
          • 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. [13]
          • 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. [14]
            • Potassium-induced aldosterone production was not found to be influenced by BMP-6. [15]
          • BMP receptor type II
            in adrenal_cortex
            • Specifically, secretion of aldosterone, was reduced by BMP-2 and BMP-5 in a dose-dependent manner. [16]
            • 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. [16]
          • 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. [17]
            • ANP-dependent decreases in aldosterone secretion from the adrenal gland require reductions in cAMP concentrations. [18]
            • ANP-dependent activation of NPR-A produces cGMP and stimulates cAMP-hydrolyzing PDE2. [18]
          • 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. [17]
          • 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. [17]
          • 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. [19]
          • 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. [19]
          • 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. [20]
          • 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. [21]


        Cellmineralcorticoid receptor
        cardiac myocyte Present
        cerebellum Present
        epidermis Present
        epithelial cell Present
        • multicellular organismal water homeostasis
        hippocampus Present
        kidney Present
        • Hypoaldosteronism
        • Primary Hyperaldosteronism
        macrophage Present
        • positive regulation of immune response
        • fibrosis
        • production of molecular mediator involved in inflammatory
        • atherosclerosis
        • hypertension
        major salivary glands Present
        microglial cell in central nervous system Present
        • positive regulation of immune response
        spleen Present