Aldosterone primarily targets the mineralocorticoid receptor (MR), a cytoplasmic/nuclear receptor that mediates the hormone's effects on electrolyte and water balance. Upon binding and activation of MR, aldosterone regulates the expression of genes involved in sodium reabsorption and potassium excretion in the kidney. The compound also activates MCR (mineralocorticoid receptor, MR), upregulating Nox-2, Nox-4, and Cox-2 to induce O2- production. Aldosterone's oxidative and inflammatory effects have been shown to affect glucose metabolism.

In vascular smooth muscle cells, interleukin-1β-stimulated nitrite generation is dose-dependently inhibited by aldosterone (1–1000 nM; 24 hours) [3]
In vitro, aldosterone (1-1000 nM; 24 hours) dose-dependently inhibits interleukin-1β-stimulated nitrite production in vascular smooth muscle cells. This demonstrates its anti-inflammatory effects in the vasculature. Aldosterone's activity is dependent on the binding and activation of the mineralocorticoid receptor at the cellular level. It has been shown to induce oxidative stress through the upregulation of Nox-2, Nox-4, and Cox-2.

Systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular systolic blood pressure (LVSP), and left ventricular end-diastolic pressure (LVEDP) are all markedly increased by aldosterone (1 mg/Kg + 1% NaCl; ih; once daily for 3 weeks) [4]. In male mice, aldosterone (0.72 mg/kg/day; 14 days) slightly raises blood pressure (14 mmHg) [5].
In vivo, aldosterone is a key regulator of electrolyte and water balance. It increases renal sodium retention and potassium excretion. Aldosterone (1 mg/kg + 1% NaCl) has been studied for its effects on left ventricular end-diastolic pressure (LVEDP). The hormone plays a significant role in the multi-factorial regulation of salt, potassium, blood pressure, and acid-base balance. It is also involved in maternal volume expansion during fetal development to support fetal perfusion.

Cell-free assays for aldosterone involve studying its binding affinity to the mineralocorticoid receptor. Radioligand binding assays are performed using purified MR protein or membrane preparations from cells expressing MR. Aldosterone is incubated with MR and a radiolabeled MR ligand. Competition binding experiments determine binding affinity. Receptor activation can be assessed using cell-free transcription assays measuring MR-mediated gene expression. The compound's chemical identity is confirmed by HPLC and mass spectrometry.

In vitro cellular assays for aldosterone typically involve treating cells expressing mineralocorticoid receptors with various concentrations of aldosterone (1-1000 nM) for defined periods (e.g., 24 hours). Nitrite production is measured using the Griess reagent to assess inflammatory responses. Oxidative stress markers are measured using fluorescent probes. Gene expression changes are assessed by qPCR. Cell viability is evaluated to ensure that the observed effects are not due to cytotoxicity.

Animal/Disease Models: Forty male Wistar rats[4]
Doses: 1 mg/Kg (+1% NaCl)
Route of Administration: ih; one time/day for 3 weeks
Experimental Results: Systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular systolic pressure (LVSP) and left ventricular end-diastolic pressure (LVEDP) were Dramatically higher in aldosterone-salt-treated animals.
In vivo animal studies for aldosterone are conducted in rodent models to study its effects on blood pressure, electrolyte balance, and cardiovascular function. The compound is administered via various routes including subcutaneous or intraperitoneal injection, often in combination with 1% NaCl in drinking water. Blood pressure is measured using telemetry or tail-cuff methods. Electrolyte levels in plasma and urine are measured. Cardiovascular parameters including left ventricular end-diastolic pressure are assessed.

Pharmacokinetic properties of aldosterone include a molecular weight of 360.44 g/mol and molecular formula C21H28O5. As a steroid hormone, it is lipophilic and has good oral bioavailability. Aldosterone is secreted by the adrenal cortex and has a short half-life in circulation. It is metabolized in the liver and excreted in urine. The compound is typically stored at appropriate conditions as a reference standard. Detailed ADME parameters are available from endocrinology studies.

The toxicity profile of aldosterone is related to its physiological role as a hormone. Excess aldosterone can lead to hypertension, hypokalemia, and cardiovascular damage. The compound is used as a research tool and reference standard, not as a therapeutic agent. Standard safety precautions should be followed when handling this compound. It is intended for research use only.

[1]. Nanba K, et al. Aging and Adrenal Aldosterone Production. Hypertension. 2018 Feb;71(2):218-223.
[2]. Cannavo A, et al. Aldosterone and Mineralocorticoid Receptor System in Cardiovascular Physiology and Pathophysiology. Oxid Med Cell Longev. 2018 Sep 19;2018:1204598.
[3]. Ikeda U, et al. Aldosterone inhibits nitric oxide synthesis in rat vascular smooth muscle cells induced by interleukin-1 beta. Eur J Pharmacol. 1995 Jul 18;290(2):69-73.
[4]. Martín-Fernández B, et al. Beneficial effects of proanthocyanidins in the cardiac alterations induced by aldosterone in ratheart through mineralocorticoid receptor blockade. PLoS One. 2014 Oct 29;9(10):e111104.
[5]. Dinh QN, et al. Aldosterone-induced oxidative stress and inflammation in the brain are mediated by the endothelial cell mineralocorticoid receptor. Brain Res. 2016 Apr 15;1637:146-153.

Aldosterone is a pregnane steroid hormone secreted by the outer layer of the adrenal cortex (zona glomerulosa). It acts on the distal convoluted tubules and collecting ducts of the kidneys, promoting sodium reabsorption, potassium excretion, water retention, and increased blood pressure. The overall function of aldosterone is to increase the reabsorption of ions and water by the kidneys. It is a metabolite in both humans and mice. Aldosterone is a 11β-hydroxysteroid, 21-hydroxysteroid, 18-oxosteroid, 20-oxosteroid, C21-steroid hormone, steroidal aldehyde, 3-oxo-Δ4 steroid, primary α-hydroxyketone, and mineralocorticoid. It is derived from the hydrogenation of pregnane.
A hormone secreted by the adrenal cortex, it regulates electrolyte and water balance by increasing the renal reabsorption of sodium and potassium excretion.
Aldosterone is present in or produced by Escherichia coli (K12 strain, MG1655 strain).
There are reports and data regarding the presence of aldosterone in the human body.
Aldosterone is a mineralocorticoid hormone synthesized by aldosterone synthase (CYP11B2) in the zona glomerulosa of the adrenal cortex. Aldosterone binds to the mineralocorticoid receptor (MR; NR3C2), forming the MR-aldosterone complex, which regulates gene expression involved in sodium retention, potassium secretion, and water reabsorption, all of which may contribute to elevated blood pressure.
Aldosterone is a hormone secreted by the adrenal cortex that regulates electrolyte and water balance by increasing renal sodium retention and potassium excretion.

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Pharmacodynamics
In the distal convoluted tubule and collecting duct, aldosterone mainly plays two roles: 1) Aldosterone acts on the mineralocorticoid receptor (MR) on the chief cells of the distal convoluted tubule of the nephron, increasing the permeability of its apical membrane (luminal side) to potassium and sodium, and activating the Na+/K+ pump on its basolateral membrane, stimulating ATP hydrolysis, leading to pump phosphorylation, and causing a conformational change in the pump, thereby exposing Na+. The aldosterone pump then expels the ions from the body.
The phosphorylated form of the aldosterone pump has a low affinity for sodium ions (Na+), thus reabsorbing sodium ions (Na+) and water back into the blood and secreting potassium ions (K+) into the urine; 2) Aldosterone stimulates intercalated cells in the collecting duct to secrete hydrogen ions (H+), regulating plasma bicarbonate (HCO3−) levels and its acid-base balance; 3) Aldosterone may act on the central nervous system through the posterior pituitary gland to release vasopressin (ADH), which retains water by directly acting on renal tubular reabsorption.
Aldosterone is a steroid hormone produced by the adrenal cortex that regulates electrolyte balance, blood pressure, and fluid homeostasis by activating mineralocorticoid receptors. It increases renal sodium retention and potassium excretion. In vitro, aldosterone (1-1000 nM) inhibits IL-1β-stimulated nitrite production in vascular smooth muscle cells. Aldosterone is a key hormone in cardiovascular and renal physiology and serves as a research tool for studying mineralocorticoid receptor signaling.

C21H28O5

360.44402

360.193

52-39-1

5839

White to off-white solid powder

1.3±0.1 g/cm3

568.1±50.0 °C at 760 mmHg

170-172ºC

311.4±26.6 °C

0.0±3.5 mmHg at 25°C

1.586

0.73

2

5

3

26

682

7

C[C@@]12CCC(=O)C=C2CC[C@H]3[C@@H]4CC[C@H](C(=O)CO)[C@]4(C[C@@H]([C@@H]31)O)C=O

PQSUYGKTWSAVDQ-ZVIOFETBSA-N

InChI=1S/C21H28O5/c1-20-7-6-13(24)8-12(20)2-3-14-15-4-5-16(18(26)10-22)21(15,11-23)9-17(25)19(14)20/h8,11,14-17,19,22,25H,2-7,9-10H2,1H3/t14-,15-,16+,17-,19+,20-,21+/m0/s1

(8S,9S,10R,11S,13R,14S,17S)-11-hydroxy-17-(2-hydroxyacetyl)-10-methyl-3-oxo-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthrene-13-carbaldehyde

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (~277.44 mM)
Ethanol : ~33.33 mg/mL (~92.47 mM)

Solubility in Formulation 1: ≥ 2.5 mg/mL (6.94 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (6.94 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (6.94 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: ≥ 2.5 mg/mL (6.94 mM) (saturation unknown) in 10% EtOH + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 400 μL of PEG300 and mix evenly; then add 50 μL of Tween-80 to the above solution and mix evenly; then add 450 μL of normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 5: ≥ 2.5 mg/mL (6.94 mM) (saturation unknown) in 10% EtOH + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 6: ≥ 2.5 mg/mL (6.94 mM) (saturation unknown) in 10% EtOH + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear EtOH stock solution to 900 μL of corn oil and mix evenly.

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 (Please use freshly prepared in vivo formulations for optimal results.)