Aldosterone - wikipedia Aldosterone Aldosterone Names IUPAC name 11β, 21 - Dihydroxy - 3, 20 - dioxopregn - 4 - en - 18 - al Identifiers CAS Number 52 - 39 - 1 3D model ( JSmol ) Interactive image ChEBI CHEBI : 27584 ChEMBL ChEMBL273453 ChemSpider 5633 DrugBank DB04630 ECHA InfoCard 100.000. 128 IUPHAR / BPS 2872 KEGG D10528 MeSH Aldosterone PubChem CID 5839 InChI 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 Key : PQSUYGKTWSAVDQ - ZVIOFETBSA - N InChI = 1 / 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 Key : PQSUYGKTWSAVDQ - ZVIOFETBBV SMILES O = C ( CO ) ( C @ @ H ) 4 ( C @ @ ) 3 ( C = O ) C ( C@H ) ( O ) ( C @ @ H ) 2 ( C @ @ ) 1 ( / C ( = C C ( = O ) CC1 ) CC ( C@H ) 2 ( C @ @ H ) 3CC4 ) C Properties Chemical formula Molar mass 360.45 g mol Pharmacology ATC code H02AA01 ( WHO ) Except where otherwise noted, data are given for materials in their standard state ( at 25 ° C ( 77 ° F ), 100 kPa ). N verify ( what is ? ) Infobox references Aldosterone, the main mineralocorticoid hormone, is a steroid hormone produced by the zona glomerulosa of the adrenal cortex in the adrenal gland. It is essential for sodium conservation in the kidney, salivary glands, sweat glands and colon. It plays a central role in the homeostatic regulation of blood pressure, plasma sodium ( Na ), and potassium ( K ) levels. It does so mainly by acting on the mineralocorticoid receptors in the distal tubules and collecting ducts of the nephron. It influences the reabsorption of sodium and excretion of potassium ( from and into the tubular fluids, respectively ) of the kidney, thereby indirectly influencing water retention or loss, blood pressure and blood volume. When dysregulated, aldosterone is pathogenic and contributes to the development and progression of cardiovascular and renal disease. Aldosterone has exactly the opposite function of the atrial natriuretic hormone secreted by the heart. Aldosterone is part of the renin -- angiotensin -- aldosterone system. It has a plasma half - life of under 20 minutes. Drugs that interfere with the secretion or action of aldosterone are in use as antihypertensives, like lisinopril, which lowers blood pressure by blocking the angiotensin - converting enzyme ( ACE ), leading to lower aldosterone secretion. The net effect of these drugs is to reduce sodium and water retention but increase retention of potassium. In other words, these drugs stimulate the excretion of sodium and water in urine, while they block the excretion of potassium. Another example is spironolactone, a potassium - sparing diuretic of the steroidal spirolactone group, which decreases blood pressure by releasing fluid from the body while retaining potassium. Aldosterone was first isolated by Simpson and Tait in 1953. Contents 1 Biosynthesis 1.1 Stimulation 2 Biological function 3 Mineralocorticoid receptors 4 Control of aldosterone release from the adrenal cortex 4.1 Major regulators 4.1. 1 The role of the renin -- angiotensin system 4.1. 2 The plasma concentration of potassium 4.1. 3 Adrenocorticotropic hormone 4.2 Miscellaneous regulators 4.2. 1 The role of sympathetic nerves 4.2. 2 The role of baroreceptors 4.2. 3 The plasma concentration of sodium 4.3 Aldosterone feedback 5 Associated clinical conditions 5.1 Hyperaldosteronism 5.2 Hypoaldosteronism 6 Additional images 7 See also 8 References 9 External links Biosynthesis The corticosteroids are synthesized from cholesterol within the zona glomerulosa of adrenal cortex. Most steroidogenic reactions are catalysed by enzymes of the cytochrome P450 family. They are located within the mitochondria and require adrenodoxin as a cofactor ( except 21 - hydroxylase and 17α - hydroxylase ). Aldosterone and corticosterone share the first part of their biosynthetic pathways. The last parts are mediated either by the aldosterone synthase ( for aldosterone ) or by the 11β - hydroxylase ( for corticosterone ). These enzymes are nearly identical ( they share 11β - hydroxylation and 18 - hydroxylation functions ), but aldosterone synthase is also able to perform an 18 - oxidation. Moreover, aldosterone synthase is found within the zona glomerulosa at the outer edge of the adrenal cortex ; 11β - hydroxylase is found in the zona glomerulosa and zona fasciculata. Steroidogenesis, showing aldosterone synthesis at upper - right corner. Note : aldosterone synthase is absent in other sections of the adrenal gland. Stimulation Aldosterone synthesis is stimulated by several factors : increase in the plasma concentration of angiotensin III, a metabolite of angiotensin II increase in plasma angiotensin II, ACTH, or potassium levels, which are present in proportion to plasma sodium deficiencies. ( The increased potassium level works to regulate aldosterone synthesis by depolarizing the cells in the zona glomerulosa, which opens the voltage - dependent calcium channels. ) The level of angiotensin II is regulated by angiotensin I, which is in turn regulated by renin, a hormone secreted in the kidneys. Serum potassium concentrations are the most potent stimulator of aldosterone secretion. the ACTH stimulation test, which is sometimes used to stimulate the production of aldosterone along with cortisol to determine whether primary or secondary adrenal insufficiency is present. However, ACTH has only a minor role in regulating aldosterone production ; with hypopituitarism there is no atrophy of the zona glomerulosa. plasma acidosis the stretch receptors located in the atria of the heart. If decreased blood pressure is detected, the adrenal gland is stimulated by these stretch receptors to release aldosterone, which increases sodium reabsorption from the urine, sweat, and the gut. This causes increased osmolarity in the extracellular fluid, which will eventually return blood pressure toward normal. adrenoglomerulotropin, a lipid factor, obtained from pineal extracts. It selectively stimulates secretion of aldosterone. The secretion of aldosterone has a diurnal rhythm. Biological function Aldosterone is the primary of several endogenous members of the class of mineralocorticoids in humans. Deoxycorticosterone is another important member of this class. Aldosterone tends to promote Na and water retention, and lower plasma K concentration by the following mechanisms : Acting on the nuclear mineralocorticoid receptors ( MR ) within the principal cells of the distal tubule and the collecting duct of the kidney nephron, it upregulates and activates the basolateral Na / K pumps, which pumps three sodium ions out of the cell, into the interstitial fluid and two potassium ions into the cell from the interstitial fluid. This creates a concentration gradient which results in reabsorption of sodium ( Na ) ions and water ( which follows sodium ) into the blood, and secreting potassium ( K ) ions into the urine ( lumen of collecting duct ). Aldosterone upregulates epithelial sodium channels ( ENaCs ) in the collecting duct and the colon, increasing apical membrane permeability for Na and thus absorption. Cl is reabsorbed in conjunction with sodium cations to maintain the system 's electrochemical balance. Aldosterone stimulates the secretion of K into the tubular lumen. Aldosterone stimulates Na and water reabsorption from the gut, salivary and sweat glands in exchange for K. Aldosterone stimulates secretion of H via the H+ / ATPase in the intercalated cells of the cortical collecting tubules Aldosterone upregulates expression of NCC in the distal convoluted tubule chronically and its activity acutely. Aldosterone is responsible for the reabsorption of about 2 % of filtered sodium in the kidneys, which is nearly equal to the entire sodium content in human blood under normal glomerular filtration rates. Aldosterone, probably acting through mineralocorticoid receptors, may positively influence neurogenesis in the dentate gyrus. Mineralocorticoid receptors Steroid receptors are intracellular. The aldosterone mineralocorticoid receptor ( MR ) complex binds on the DNA to specific hormone response element, which leads to gene specific transcription. Some of the transcribed genes are crucial for transepithelial sodium transport, including the three subunits of the epithelial sodium channel ( ENaC ), the Na / K pumps and their regulatory proteins serum and glucocorticoid - induced kinase, and channel - inducing factor, respectively. The MR is stimulated by both aldosterone and cortisol, but a mechanism protects the body from excess aldosterone receptor stimulation by glucocorticoids ( such as cortisol ), which happen to be present at much higher concentrations than mineralocorticoids in the healthy individual. The mechanism consists of an enzyme called 11 β - hydroxysteroid dehydrogenase ( 11β - HSD ). This enzyme co-localizes with intracellular adrenal steroid receptors and converts cortisol into cortisone, a relatively inactive metabolite with little affinity for the MR. Liquorice, which contains glycyrrhetinic acid, can inhibit 11β - HSD and lead to a mineralocorticoid excess syndrome. Control of aldosterone release from the adrenal cortex The renin -- angiotensin system, showing role of aldosterone between the adrenal glands and the kidneys Major regulators The role of the renin -- angiotensin system Angiotensin is involved in regulating aldosterone and is the core regulation. Angiotensin II acts synergistically with potassium, and the potassium feedback is virtually inoperative when no angiotensin II is present. A small portion of the regulation resulting from angiotensin II must take place indirectly from decreased blood flow through the liver due to constriction of capillaries. When the blood flow decreases so does the destruction of aldosterone by liver enzymes. Although sustained production of aldosterone requires persistent calcium entry through low - voltage - activated Ca channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca channels entry. However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity ; this innate electrical excitability of zona glomerulosa cells provides a platform for the production of a recurrent Ca channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production. Voltage - gated Ca channels have been detected in the zona glomerulosa of the human adrenal, which suggests that Ca channel blockers may directly influence the adrenocortical biosynthesis of aldosterone in vivo. The plasma concentration of potassium The amount of aldosterone secreted is a direct function of the serum potassium as probably determined by sensors in the carotid artery. Adrenocorticotropic hormone Adrenocorticotropic hormone ( ACTH ), a pituitary peptide, also has some stimulating effect on aldosterone, probably by stimulating the formation of deoxycorticosterone, a precursor of aldosterone. Aldosterone is increased by blood loss, pregnancy, and possibly by further circumstances such as physical exertion, endotoxin shock, and burns. Miscellaneous regulators The role of sympathetic nerves The aldosterone production is also affected to one extent or another by nervous control, which integrates the inverse of carotid artery pressure, pain, posture, and probably emotion ( anxiety, fear, and hostility ) ( including surgical stress ). Anxiety increases aldosterone, which must have evolved because of the time delay involved in migration of aldosterone into the cell nucleus. Thus, there is an advantage to an animal 's anticipating a future need from interaction with a predator, since too high a serum content of potassium has very adverse effects on nervous transmission. The role of baroreceptors Pressure - sensitive baroreceptors are found in the vessel walls of nearly all large arteries in the thorax and neck, but are particularly plentiful in the sinuses of the carotid arteries and in the arch of the aorta. These specialized receptors are sensitive to changes in mean arterial pressure. An increase in sensed pressure results in an increased rate of firing by the baroreceptors and a negative feedback response, lowering systemic arterial pressure. Aldosterone release causes sodium and water retention, which causes increased blood volume, and a subsequent increase in blood pressure, which is sensed by the baroreceptors. To maintain normal homeostasis these receptors also detect low blood pressure or low blood volume, causing aldosterone to be released. This results in sodium retention in the kidney, leading to water retention and increased blood volume. The plasma concentration of sodium Aldosterone is a function of the inverse of the sodium intake as sensed via osmotic pressure. The slope of the response of aldosterone to serum potassium is almost independent of sodium intake. Aldosterone is increased at low sodium intakes, but the rate of increase of plasma aldosterone as potassium rises in the serum is not much lower at high sodium intakes than it is at low. Thus, the potassium is strongly regulated at all sodium intakes by aldosterone when the supply of potassium is adequate, which it usually is in primitive diets. Aldosterone feedback Feedback by aldosterone concentration itself is of a nonmorphological character ( that is, other than changes in the cells ' number or structure ) and is poor, so the electrolyte feedbacks predominate, short term. Associated clinical conditions Hyperaldosteronism is abnormally increased levels of aldosterone, while hypoaldosteronism is abnormally decreased levels of aldosterone. A measurement of aldosterone in blood may be termed a plasma aldosterone concentration ( PAC ), which may be compared to plasma renin activity ( PRA ) as an aldosterone - to - renin ratio. Hyperaldosteronism Primary aldosteronism, also known as primary hyperaldosteronism, is characterized by the overproduction of aldosterone by the adrenal glands, when not a result of excessive renin secretion. It leads to arterial hypertension ( high blood pressure ) associated with hypokalemia, usually a diagnostic clue. Secondary hyperaldosteronism, on the other hand, is due to overactivity of the renin -- angiotensin system. Conn 's syndrome is primary hyperaldosteronism caused by an aldosterone - producing adenoma. Depending on cause and other factors, hyperaldosteronism can be treated by surgery and / or medically, such as by aldosterone antagonists. Hypoaldosteronism An ACTH stimulation test for aldosterone can help in determining the cause of hypoaldosteronism, with a low aldosterone response indicating a primary hypoaldosteronism of the adrenals, while a large response indicating a secondary hypoaldosteronism. Additional images Corticosteroid biosynthetic pathway in rat Corticosterone See also Mineralocorticoid References Jump up ^ Jaisser F, Farman N ( January 2016 ). `` Emerging Roles of the Mineralocorticoid Receptor in Pathology ''. Pharmacological Reviews. 68 : 49 -- 75. doi : 10.1124 / pr. 115.011106. Jump up ^ Marieb, Elaine Nicpon ; Hoehn, Katja ( 2013 ). `` Chapter 16 ''. Human anatomy & physiology ( 9th ed. ). Boston : Pearson. pp. 629, Question 14. OCLC 777127809. ^ Jump up to : Arai, Keiko ; Chrousos, George P. ( 2000 - 01 - 01 ). `` Aldosterone Deficiency and Resistance ''. 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External links Aldosterone at Lab Tests Online Hormones Endocrine glands Hypothalamic - pituitary Hypothalamus GnRH TRH Dopamine CRH GHRH Somatostatin ( GHIH ) MCH Posterior pituitary Oxytocin Vasopressin Anterior pituitary FSH LH TSH Prolactin POMC CLIP ACTH MSH Endorphins Lipotropin GH Adrenal axis Adrenal cortex aldosterone cortisol cortisone DHEA DHEA - S androstenedione Adrenal medulla epinephrine norepinephrine Thyroid Thyroid hormone Calcitonin Thyroid axis Parathyroid PTH Gonadal axis Testis testosterone AMH inhibin Ovary estradiol progesterone activin and inhibin relaxin Placenta hCG HPL estrogen progesterone Pancreas glucagon insulin amylin somatostatin pancreatic polypeptide Pineal gland melatonin N, N - dimethyltryptamine 5 - methoxy - N, N - dimethyltryptamine Other Thymus Thymosins Thymosin α1 Beta thymosins Thymopoietin Thymulin Digestive system Stomach gastrin ghrelin Duodenum CCK Incretins GIP GLP - 1 secretin motilin VIP Ileum enteroglucagon peptide YY Liver / other Insulin - like growth factor IGF - 1 IGF - 2 Adipose tissue leptin adiponectin resistin Skeleton Osteocalcin Kidney renin EPO calcitriol prostaglandin Heart Natriuretic peptide ANP BNP Endogenous steroids Precursors Cholesterol 22R - Hydroxycholesterol 20α, 22R - Dihydroxycholesterol Pregnenolone 11β - Hydroxypregnenolone 17α - Hydroxypregnenolone 21 - Hydroxypregnenolone 17α, 21 - Dihydroxypregnenolone 11β, 17α, 21 - Trihydroxypregnenolone Corticosteroids Glucocorticoids 3α, 5α - Tetrahydrocorticosterone 5α - Dihydrocorticosterone 11 - Deoxycorticosterone 11 - Deoxycortisol 11 - Ketoprogesterone 21 - Deoxycortisol 21 - Deoxycortisone Corticosterone Cortisol Cortisone 17α - Hydroxypregnenolone 17α - Hydroxyprogesterone Pregnenolone Progesterone Mineralocorticoids 5α - Dihydroaldosterone 11 - Dehydrocorticosterone ( 11 - oxocorticosterone, 17 - deoxycortisone ) 11 - Deoxycortisol 11 - Deoxycorticosterone 11β - Hydroxyprogesterone ( 21 - deoxycorticosterone ) 18 - Hydroxy - 11 - deoxycorticosterone 18 - Hydroxycorticosterone 18 - Hydroxyprogesterone Aldosterone Corticosterone Cortisol Sex steroids Androgens 11 - Ketodihydrotestosterone 11 - Ketotestosterone 7β - Hydroxyepiandrosterone 11β - Hydroxyandrostenedione Adrenosterone ( 11 - ketoandrostenedione ) Androstenediol Androstenedione Androsterone Dehydroandrosterone DHEA DHEA sulfate Dihydrotestosterone Epiandrosterone Epitestosterone 16α - Hydroxyandrostenedione 16α - Hydroxy - DHEA 16α - Hydroxy - DHEA sulfate Testosterone Metabolites : 3α - Androstanediol 3α - Androstanediol glucuronide 3β - Androstanediol 3α, 5β - Androstanediol 3β, 5β - Androstanediol 5β - Androstanedione 5β - Dihydrotestosterone Androstanetriols Androstenediol sulfate Androsterone glucuronide Androsterone sulfate Dihydrotestosterone glucuronide Dihydrotestosterone sulfate Etiocholanolone Etiocholanolone glucuronide Epietiocholanolone Testosterone glucuronide Testosterone sulfate Estrogens Estranes : Estetrol Estradiol Estrone Estriol 17α - Estradiol 16β - Epiestriol ( 16β - hydroxyestradiol ) 17α - Epiestriol ( 16α - hydroxy - 17α - estradiol ) 16β, 17α - Epiestriol ( 16β - hydroxy - 17α - estradiol ) 2 - Hydroxyestradiol 2 - Hydroxyestriol 2 - Hydroxyestrone 4 - Hydroxyestradiol 4 - Hydroxyestriol 4 - Hydroxyestrone 4 - Methoxyestradiol 16α - Hydroxyestrone Others : 27 - Hydroxycholesterol 3α - Androstanediol 3β - Androstanediol 4 - Androstenedione 5 - Androstenediol DHEA DHEA sulfate 7 - Keto - DHEA 7α - Hydroxy - DHEA 16α - Hydroxy - DHEA Metabolites : 2 - Methoxyestradiol 2 - Methoxyestrone 4 - Methoxyestrone Estradiol glucuronide Estradiol sulfate Estrone glucuronide Estrone sulfate Estriol glucuronide Estriol sulfate Lipoidal estradiol ( e.g., estradiol stearate, estradiol palmitate ) Progestogens Progesterone 16α - Hydroxyprogesterone 17α - Hydroxyprogesterone 20α - Dihydroprogesterone 5α - Dihydroprogesterone 11 - Deoxycorticosterone 5α - DHDOC Metabolites : Allopregnanediol Pregnanediol Pregnanediol glucuronide Pregnanetriol Neurosteroids Cholestanes : 24S - Hydroxycholesterol Cholesterol Pregnanes : 3α - Dihydroprogesterone 3β - Dihydroprogesterone 5α - Dihydrocorticosterone 5α - Dihydroprogesterone 5β - Dihydroprogesterone Allopregnanolone Corticosterone DHC DHDOC 11 - Deoxycorticosterone Epipregnanolone Isopregnanolone Pregnanolone Pregnenolone Pregnenolone sulfate Progesterone THB THDOC Androstanes : 3α - Androstanediol 3α - Androstenol 7 - Keto - DHEA 7α - Hydroxy - DHEA 7β - Hydroxy - DHEA 7α - Hydroxyepiandrosterone 7β - Hydroxyepiandrosterone Androsterone DHEA DHEA sulfate Etiocholanolone Pheromones : 3α - Androstenol 3β - Androstenol Androstadienol Androstadienone Androstenone Androsterone Estratetraenol Others Vitamin D: 7 - Dehydrocholesterol Calcidiol / Calcifediol Calcitriol Cholecalciferol Others : 7α - Hydroxycholesterol 11α - Hydroxyprogesterone 11β - Hydroxyprogesterone Cholesterol sulfate Physiology of the kidneys and acid - base physiology Renal function Secretion clearance Pharmacokinetics Clearance of medications Urine flow rate Reabsorption Solvent drag sodium chloride urea glucose oligopeptides protein Renal function Glomerular filtration rate Creatinine clearance Renal clearance ratio Urea reduction ratio Kt / V Standardized Kt / V Measures of dialysis Hemodialysis product PAH clearance ( Effective renal plasma flow Extraction ratio ) Filtration Renal blood flow Ultrafiltration Countercurrent exchange Filtration fraction Hormones Antidiuretic hormone Aldosterone Atrial natriuretic peptide Renin Erythropoietin Calcitriol Prostaglandins Acid - base balance Fluid balance Darrow Yannet diagram Body water : Intracellular fluid / Cytosol Extracellular fluid ( Interstitial fluid Plasma Transcellular fluid ) Base excess Davenport diagram Anion gap Arterial blood gas Winters ' formula Buffering Bicarbonate buffer system Respiratory compensation Renal compensation Other Fractional sodium excretion BUN - to - creatinine ratio Tubuloglomerular feedback Natriuresis Urine Mineralocorticoids and antimineralocorticoids ( H02 ) Mineralocorticoids Desoxycortone ( desoxycorticosterone ) Desoxycortone esters Hydrocortisone ( cortisol ) Hydrocortisone esters Fludrocortisone Fludrocortisone acetate Methylprednisolone Methylprednisolone esters Prednisolone Prednisolone esters Prednisone Prednisone esters Antimineralocorticoids Steroidal : Canrenoate potassium ( potassium canrenoate ) Canrenone Drospirenone Dydrogesterone Eplerenone Gestodene Medrogestone Progesterone Spironolactone Trimegestone Nonsteroidal : Amlodipine Apararenone Benidipine Esaxerenone Felodipine Finerenone Nifedipine Nimodipine Nitrendipine Synthesis modifiers Acetoxolone Aminoglutethimide Carbenoxolone Enoxolone Ketoconazole Metyrapone Mitotane Trilostane WHO - EM Withdrawn from market Clinical trials : Phase III Never to phase III See also Mineralocorticoid receptor modulators Glucocorticoids and antiglucocorticoids List of corticosteroids Mineralocorticoid receptor modulators MR Agonists 11 - Dehydrocorticosterone ( 11 - oxocorticosterone, 17 - deoxycortisone ) 11 - Dehydrocorticosterone acetate 11 - Deoxycorticosterone ( desoxycortone, deoxycortone, desoxycorticosterone ) Desoxycortone esters 11 - Deoxycortisol ( cortodoxone, cortexolone ) Cortifen ( cortiphen, kortifen ) Cortodoxone acetate 11β - Hydroxyprogesterone 16α, 18 - Dihydroxy - 11 - deoxycorticosterone 17α - Hydroxyaldosterone 18 - Hydroxy - 11 - deoxycorticosterone 19 - Norprogesterone Aldosterone Corticosterone Corticosterone acetate Corticosterone benzoate Cortisol ( hydrocortisone ) Benzodrocortisone ( hydrocortisone benzoate ) Hydrocortamate ( hydrocortisone diethylaminoacetate ) Hydrocortisone esters Cortisone Cortisone acetate Fludrocortisone ( fludrocortone ) Fludrocortisone acetate Mometasone Mometasone furoate Prednisolone Prednazate Prednazoline Prednicarbate ( prednisolone ethylcarbonate propionate ) Prednimustine Prednisolamate ( prednisolone diethylaminoacetate ) Prednisolone esters Prednisone Prednisone esters Antagonists Steroidal : 6β - Hydroxy - 7α - thiomethylspironolactone 7α - Acetylthio - 17α - hydroxyprogesterone 7α - Thiomethylspironolactone ( SC - 26519 ) 7α - Thioprogesterone ( SC - 8365 ) 7α - Thiospironolactone ( SC - 24813 ) 16α - Hydroxyprogesterone 17α - Hydroxyprogesterone ( hydroxyprogesterone ) 18 - Deoxyaldosterone 18, 19 - Dinorprogesterone Canrenoate potassium ( potassium canrenoate ) Canrenoic acid ( canrenoate ) Canrenone ( canrenoate y - lactone ) Dicirenone Dimethisterone Drospirenone Dydrogesterone Eplerenone Gestodene Guggulsterone Hydroxyprogesterone caproate Medrogestone Mespirenone Metribolone Mexrenoate potassium Mexrenoic acid ( mexrenoate ) Mexrenone Oxprenoic acid ( oxprenoate ) Oxprenoate potassium ( RU - 28318 ) Pregnenolone Progesterone Prorenoate potassium Prorenoic acid ( prorenoate ) Prorenone RO - 14 - 9012 RU - 26752 SC - 5233 ( spirolactone ) SC - 8109 SC - 11927 ( CS - 1 ) SC - 19886 SC - 27169 Spirorenone Spironolactone Spiroxasone Tibolone Trimegestone ZK - 91587 ZK - 97894 Nonsteroidal : Amlodipine Apararenone Benidipine BR - 4628 Esaxerenone Felodipine Finerenone Nifedipine Nimodipine Nitrendipine PF - 03882845 SM - 368229 See also Receptor / signaling modulators Mineralocorticoids and antimineralocorticoids Glucocorticoid receptor modulators List of corticosteroids NDL : 00560334 Retrieved from `` https://en.wikipedia.org/w/index.php?title=Aldosterone&oldid=829445687 '' Categories : Mineralocorticoids Pregnanes Steroid hormones Triketones Hidden categories : Articles without UNII source ECHA InfoCard ID from Wikidata Articles with changed KEGG identifier Articles containing unverified chemical infoboxes Chembox image size set Talk Contents About Wikipedia Aragonés تۆرکجه Български Català Čeština Dansk Deutsch Ελληνικά Español Euskara فارسی Français Gaeilge Galego 한국어 Հայերեն Hrvatski Bahasa Indonesia Italiano עברית Basa Jawa Қазақша Kurdî Lietuvių Magyar Македонски Nederlands 日本 語 Norsk Occitan Oʻzbekcha / ўзбекча Polski Português Română Русский Scots Slovenčina Српски / srpski Srpskohrvatski / српскохрватски Suomi Svenska தமிழ் Türkçe Українська 中文 37 more Edit links This page was last edited on 8 March 2018, at 18 : 03. 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Question: what part of the kidney does aldosterone work on
Answer: nephron