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Aldosterone
Aldosterone is a steroid hormone produced by the adrenal glands, located on top of the kidneys. It plays a crucial role in regulating blood pressure and maintaining the balance of fluids and electrolytes by controlling sodium and potassium levels in the blood. When blood pressure drops, aldosterone is released as part of the renin-angiotensin-aldosterone system (RAAS), prompting the kidneys to retain sodium and excrete potassium, which helps increase blood volume and pressure. Abnormal levels of aldosterone can lead to health issues; high levels, known as hyperaldosteronism, can cause conditions such as hypertension and muscle weakness, while low levels, or hypoaldosteronism, may result in dehydration and low blood pressure.
There are two main types of hyperaldosteronism: primary, often caused by tumors on the adrenal glands, and secondary, which can arise from various conditions that affect blood flow or sodium levels. Additionally, certain genetic disorders can disrupt aldosterone production, leading to imbalances that affect overall health. Understanding aldosterone's function and its impact on the body is essential for addressing related health concerns and maintaining well-being.
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Full Article
Aldosterone is a corticosteroid, or steroid hormone, that is produced in the adrenal glands, which are located on top of each kidney. Aldosterone works with the hormones renin and angiotensin to balance fluids and electrolytes in the blood by regulating levels of sodium and potassium. This process helps to control blood pressure. The body can produce too much or too little aldosterone, which can lead to serious conditions such as hypertension (high blood pressure), stroke, cardiovascular disease, and other heart conditions. Blood and urine tests can detect high or low levels of aldosterone.
Overview
Aldosterone is released when blood pressure drops. This sends signals to the kidneys and colon to increase the amount of sodium in the bloodstream or potassium in the urine. Aldosterone increases blood volume by promoting sodium and water reabsorption in the kidneys, which raises blood pressure. The entire process helps to regulate pH and electrolyte levels in the blood.
Aldosterone works with the hormones renin and angiotensin to make up the renin-angiotensin-aldosterone system (RAAS). When blood flow to the kidneys is decreased (this happens when blood pressure drops) or low blood volume is detected by the body, the RAAS is alerted. Renin cleaves angiotensinogen into angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II stimulates the adrenal glands to release aldosterone. Once the hydration and salt levels in the blood return to their proper levels, renin is no longer produced, and the release of aldosterone is halted. In healthy individuals, the RAAS plays a major role in regulating blood pressure and fluid balance, working in coordination with other regulatory systems. The function of this system, however, is interrupted by elevated or decreased levels of aldosterone.
Hyperaldosteronism, also called aldosteronism, is the condition of having high levels of aldosterone. Primary aldosteronism, also called Conn’s syndrome, occurs when small tumors on the adrenal glands cause an overproduction of aldosterone. The condition results in elevated blood pressure, decreased potassium levels, high sodium levels, and increased blood volume. Symptoms of the condition include high blood pressure, headache, and muscle weakness. Research in the 2020s uncovered the role of the G protein-coupled estrogen receptor (GPER) in aldosterone-induced hypertension. Findings suggested that GPER activation by aldosterone may promote vascular dysfunction and contribute to high blood pressure independently of the mineralocorticoid receptor. This discovery significantly impacted therapeutic interventions in resistant hypertension and cardiovascular diseases linked to aldosterone excess.
Secondary aldosteronism, which is more common than primary aldosteronism, is also caused by raised levels of aldosterone. Unlike primary aldosteronism, where aldosterone production is autonomous, secondary aldosteronism is a compensatory response. This disorder can be triggered by several conditions that lower blood pressure, narrow the blood vessels, decrease blood flow to the kidneys, and drop sodium levels. It is common with other ailments, including cirrhosis of the liver with ascites, congestive heart failure, severe dehydration, nephrotic syndrome, and kidney disease.
Two rare inherited kidney disorders called Bartter syndrome and Gitelman syndrome can alter aldosterone levels. Both conditions cause people to lose too much sodium in the urine, increasing renin and aldosterone production and making the kidneys work harder to remove potassium. Symptoms of these disorders include low blood pressure, decreased blood volume, muscle weakness, muscle cramps, and fatigue.
Hypoaldosteronism is the condition of having low levels of aldosterone. It can cause dehydration, low blood pressure, decreased sodium levels, and elevated potassium levels. The rare autoimmune disease known as Addison’s disease, also known as primary adrenal insufficiency which damages the adrenal glands, can cause decreased levels of aldosterone. Symptoms of the condition include fatigue, weight loss, muscle deterioration, mood and behavior changes, and skin issues.
Bibliography
“Aldosterone.” Cleveland Clinic, 12 Sept. 2022, my.clevelandclinic.org/health/articles/24158-aldosterone. Accessed 30 Mar. 2026.
“Aldosterone Test.” MedlinePlus, 13 July 2025, medlineplus.gov/lab-tests/aldosterone-test. Accessed 30 Mar. 2026.
Amandolare, Sarah, and Jon Cooper. “Why Do You Need an Aldosterone Test?” WebMD, 19 Dec. 2024, www.webmd.com/a-to-z-guides/what-is-an-aldosterone-test. Accessed 30 Mar. 2026.
Chrousos, George P. “Hyperaldosteronism.” Medscape, 30 Jan. 2026, emedicine.medscape.com/article/920713-overview. Accessed 30 Mar. 2026.
Dogra, Prerna, et al. “Primary Aldosteronism: A Pragmatic Approach to Diagnosis and Management.” Mayo Clinic Proceedings, vol. 98, no. 8, Aug. 2023, pp. 1207–15, doi:10.1016/j.mayocp.2023.04.023. Accessed 30 Mar. 2026.
Imcaoudene, Ahmed Rateb et al. “Aldosterone Breakthrough for the Prediction of Treatment Response to Mineralocorticoid Receptor Antagonists.” Kidney Medicine, vol. 7, no. 8, Aug. 2025, 101040, doi:10.1016/j.xkme.2025.101040. Accessed 30 Mar. 2026.
LaRosa, Christopher J. “Bartter Syndrome and Gitelman Syndrome.” Merck Manual, Oct. 2024, www.merckmanuals.com/professional/pediatrics/congenital-renal-transport-abnormalities/bartter-syndrome-and-gitelman-syndrome. Accessed 30 Mar. 2026.
Li, Xuehan, et al. “G Protein-Coupled Estrogen Receptor: A Promising Therapeutic Target for Aldosterone-Induced Hypertension.” Frontiers in Endocrinology, vol. 14, 17 Aug. 2023, p. 1226458, doi:10.3389/fendo.2023.1226458. Accessed 30 Mar. 2026.
Pilz, Stefan, et al. “Primary Aldosteronism 2.0: An Update for Clinicians on Diagnosis and Treatment.” Polish Archives of Internal Medicine, vol. 133, no. 10, 26 Oct. 2023, doi:10.20452/pamw.16585. Accessed 30 Mar. 2026.
Rossi, Gian Paolo, et al. “Clinical Management of Primary Aldosteronism: An Update.” Hypertension, vol. 81, no. 9, Sept. 2024, pp. 1845–56, doi:10.1161/HYPERTENSIONAHA.124.22642. Accessed 30 Mar. 2026.
Full Article
Aldosterone is a corticosteroid, or steroid hormone, that is produced in the adrenal glands, which are located on top of each kidney. Aldosterone works with the hormones renin and angiotensin to balance fluids and electrolytes in the blood by regulating levels of sodium and potassium. This process helps to control blood pressure. The body can produce too much or too little aldosterone, which can lead to serious conditions such as hypertension (high blood pressure), stroke, cardiovascular disease, and other heart conditions. Blood and urine tests can detect high or low levels of aldosterone.
Overview
Aldosterone is released when blood pressure drops. This sends signals to the kidneys and colon to increase the amount of sodium in the bloodstream or potassium in the urine. Aldosterone increases blood volume by promoting sodium and water reabsorption in the kidneys, which raises blood pressure. The entire process helps to regulate pH and electrolyte levels in the blood.
Aldosterone works with the hormones renin and angiotensin to make up the renin-angiotensin-aldosterone system (RAAS). When blood flow to the kidneys is decreased (this happens when blood pressure drops) or low blood volume is detected by the body, the RAAS is alerted. Renin cleaves angiotensinogen into angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE). Angiotensin II stimulates the adrenal glands to release aldosterone. Once the hydration and salt levels in the blood return to their proper levels, renin is no longer produced, and the release of aldosterone is halted. In healthy individuals, the RAAS plays a major role in regulating blood pressure and fluid balance, working in coordination with other regulatory systems. The function of this system, however, is interrupted by elevated or decreased levels of aldosterone.
Hyperaldosteronism, also called aldosteronism, is the condition of having high levels of aldosterone. Primary aldosteronism, also called Conn’s syndrome, occurs when small tumors on the adrenal glands cause an overproduction of aldosterone. The condition results in elevated blood pressure, decreased potassium levels, high sodium levels, and increased blood volume. Symptoms of the condition include high blood pressure, headache, and muscle weakness. Research in the 2020s uncovered the role of the G protein-coupled estrogen receptor (GPER) in aldosterone-induced hypertension. Findings suggested that GPER activation by aldosterone may promote vascular dysfunction and contribute to high blood pressure independently of the mineralocorticoid receptor. This discovery significantly impacted therapeutic interventions in resistant hypertension and cardiovascular diseases linked to aldosterone excess.
Secondary aldosteronism, which is more common than primary aldosteronism, is also caused by raised levels of aldosterone. Unlike primary aldosteronism, where aldosterone production is autonomous, secondary aldosteronism is a compensatory response. This disorder can be triggered by several conditions that lower blood pressure, narrow the blood vessels, decrease blood flow to the kidneys, and drop sodium levels. It is common with other ailments, including cirrhosis of the liver with ascites, congestive heart failure, severe dehydration, nephrotic syndrome, and kidney disease.
Two rare inherited kidney disorders called Bartter syndrome and Gitelman syndrome can alter aldosterone levels. Both conditions cause people to lose too much sodium in the urine, increasing renin and aldosterone production and making the kidneys work harder to remove potassium. Symptoms of these disorders include low blood pressure, decreased blood volume, muscle weakness, muscle cramps, and fatigue.
Hypoaldosteronism is the condition of having low levels of aldosterone. It can cause dehydration, low blood pressure, decreased sodium levels, and elevated potassium levels. The rare autoimmune disease known as Addison’s disease, also known as primary adrenal insufficiency which damages the adrenal glands, can cause decreased levels of aldosterone. Symptoms of the condition include fatigue, weight loss, muscle deterioration, mood and behavior changes, and skin issues.
Bibliography
“Aldosterone.” Cleveland Clinic, 12 Sept. 2022, my.clevelandclinic.org/health/articles/24158-aldosterone. Accessed 30 Mar. 2026.
“Aldosterone Test.” MedlinePlus, 13 July 2025, medlineplus.gov/lab-tests/aldosterone-test. Accessed 30 Mar. 2026.
Amandolare, Sarah, and Jon Cooper. “Why Do You Need an Aldosterone Test?” WebMD, 19 Dec. 2024, www.webmd.com/a-to-z-guides/what-is-an-aldosterone-test. Accessed 30 Mar. 2026.
Chrousos, George P. “Hyperaldosteronism.” Medscape, 30 Jan. 2026, emedicine.medscape.com/article/920713-overview. Accessed 30 Mar. 2026.
Dogra, Prerna, et al. “Primary Aldosteronism: A Pragmatic Approach to Diagnosis and Management.” Mayo Clinic Proceedings, vol. 98, no. 8, Aug. 2023, pp. 1207–15, doi:10.1016/j.mayocp.2023.04.023. Accessed 30 Mar. 2026.
Imcaoudene, Ahmed Rateb et al. “Aldosterone Breakthrough for the Prediction of Treatment Response to Mineralocorticoid Receptor Antagonists.” Kidney Medicine, vol. 7, no. 8, Aug. 2025, 101040, doi:10.1016/j.xkme.2025.101040. Accessed 30 Mar. 2026.
LaRosa, Christopher J. “Bartter Syndrome and Gitelman Syndrome.” Merck Manual, Oct. 2024, www.merckmanuals.com/professional/pediatrics/congenital-renal-transport-abnormalities/bartter-syndrome-and-gitelman-syndrome. Accessed 30 Mar. 2026.
Li, Xuehan, et al. “G Protein-Coupled Estrogen Receptor: A Promising Therapeutic Target for Aldosterone-Induced Hypertension.” Frontiers in Endocrinology, vol. 14, 17 Aug. 2023, p. 1226458, doi:10.3389/fendo.2023.1226458. Accessed 30 Mar. 2026.
Pilz, Stefan, et al. “Primary Aldosteronism 2.0: An Update for Clinicians on Diagnosis and Treatment.” Polish Archives of Internal Medicine, vol. 133, no. 10, 26 Oct. 2023, doi:10.20452/pamw.16585. Accessed 30 Mar. 2026.
Rossi, Gian Paolo, et al. “Clinical Management of Primary Aldosteronism: An Update.” Hypertension, vol. 81, no. 9, Sept. 2024, pp. 1845–56, doi:10.1161/HYPERTENSIONAHA.124.22642. Accessed 30 Mar. 2026.
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