Aldosterone
(Synonyms: 醛固酮) 目录号 : GC41390醛固酮是由肾上腺皮质分泌的一种类固醇激素，是控制钠和钾平衡的主要矿物质皮质激素
Cas No.:52-39-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Aldosterone is a steroid hormone secreted by the adrenal cortex and is the principle mineralocorticoid controlling sodium and potassium balance.[1],[2] Its primary role is to promote unidirectional salt reabsorption in epithelial tissues. Aldosterone is synthesized from cholesterol in the zona glomerulosa of the adrenal cortex and its secretion is regulated via the renin-angiotensin system.[3]
醛固酮是由肾上腺皮质分泌的一种类固醇激素，是控制钠和钾平衡的主要矿物质皮质激素。它的主要作用是促进上皮组织中单向盐吸收。醛固酮从胆固醇合成于肾上腺皮层的球状带，并通过肾素-血管紧张素系统调节其分泌。
Reference:
[1]. Agarwal, M.K., and Mirshahi, M. General overview of mineralocorticoid hormone action. Pharmacology & Toxicology 84, 273-326 (1999).
[2]. Rogerson, F.M., and Fuller, P.J. Mineralocorticoid action. Steroids 65, 61-73 (2000).
[3]. Lumbers, E.R. Angiotensin and aldosterone. Regulatory Peptides 80, 91-100 (1999).
| Cas No. | 52-39-1 | SDF | |
| 别名 | 醛固酮 | ||
| 化学名 | 11β,21-dihydroxy-3,20-dioxo-pregn-4-en-18-al | ||
| Canonical SMILES | O=C1CC[C@@]2(C)C(CC[C@]3([H])[C@]2([H])[C@@H](O)C[C@@]4(C([H])=O)[C@@]3([H])CC[C@@H]4C(CO)=O)=C1 | ||
| 分子式 | C21H28O5 | 分子量 | 360.4 |
| 溶解度 | 30mg/mL in DMSO, 30mg/ml in ethanol, 30mg/ml in DMF，PBS(pH 7.2) (1:1): 0.2 mg/ml ethanol | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.7747 mL | 13.8735 mL | 27.7469 mL |
| 5 mM | 0.5549 mL | 2.7747 mL | 5.5494 mL |
| 10 mM | 0.2775 mL | 1.3873 mL | 2.7747 mL |
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| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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2.
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Pathology of Aldosterone Biosynthesis and its Action
Tohoku J Exp Med 2021 May;254(1):1-15.PMID:34011803DOI:10.1620/tjem.254.1.
Aldosterone plays pivotal roles in renin-angiotensin-aldosterone system in order to maintain the equilibrium of liquid volume and electrolyte metabolism. Aldosterone action is mediated by both mineralocorticoid receptor and 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2). Its excessive actions directly induced tissue injuries in its target organs such as myocardial and vascular fibrosis in addition to chronic kidney diseases. Excessive Aldosterone actions were also reported to be involved in unbalanced electrolyte metabolism in inflammatory bowel disease and development of pulmonary diseases. Hyperaldosteronism is tentatively classified into primary and secondary types. Primary aldosteronism is more frequent and has been well known to result in secondary hypertension with subsequent cardiovascular damages. Primary aldosteronism is also further classified into distinctive subtypes and among those, aldosterone-producing adenoma is the most frequent one accounting for the great majority of unilateral primary aldosteronism cases. In bilateral hyperaldosteronism, aldosterone-producing diffuse hyperplasia and aldosterone-producing micronodules or nodules are the major subtypes. All these aldosterone-producing lesions were reported to harbor somatic mutations including KCNJ5, CACNA1D, ATP1A1 and ATP2B3, which were all related to excessive Aldosterone production. Among those mutations above, somatic mutation of KCNJ5 is the most frequent in aldosterone-producing adenoma and mostly composed of clear cells harboring abundant Aldosterone synthase expression. In contrast, CACNA1D-mutated aldosterone-producing micronodules or aldosterone-producing nodules were frequently detected not only in primary aldosteronism patients but also in the zona glomerulosa of normal adrenal glands, which could eventually lead to an autonomous Aldosterone production resulting in normotensive or overt primary aldosteronism, but their details have remained unknown.
Arterial Hypertension, Aldosterone, and Atrial Fibrillation
Curr Hypertens Rep 2019 Nov 18;21(12):94.PMID:31741119DOI:10.1007/s11906-019-1001-4.
Purpose: Atrial fibrillation is the most common sustained arrhythmia, with a prevalence of 1-2% in the general population and over 15% in people older than 80 years. Due to aging of the population it imposes an increasing burden on the healthcare system because of the need for life-long pharmacological treatment and the associated increased risk of heart failure and hospitalization. Hence, identification of the factors that predispose to atrial fibrillation it is of utmost relevance. Recent findings: Several conditions exist that are characterized by inappropriately high levels of Aldosterone, mostly primary aldosteronism and the severe or drug-resistant forms of arterial hypertension. In these forms, Aldosterone can cause prominent target organ damage, mostly in the heart, vasculature, and kidney. This review examines the experimental data and clinical evidences that support a link between hyperaldosteronism and atrial fibrillation, and how this knowledge should lead to a change in our management of the hypertensive patients presenting with atrial fibrillation.
Primary Aldosteronism, Aldosterone, and Extracellular Vesicles
Endocrinology 2022 Jan 1;163(1):bqab240.PMID:34918071DOI:10.1210/endocr/bqab240.
Primary aldosteronism (PA) is an endocrine related condition leading to arterial hypertension due to inappropriately high and unregulated Aldosterone concentration. Recently, a broad spectrum of PA has been recognized, which brings new challenges associated with early identification of this condition that affect renal epithelial and extrarenal tissues. Reports have shown the potential role of extracellular vesicles (EVs) and EV cargo as novel and complementary biomarkers in diagnosis and prognosis of PA. In vivo and in vitro studies have identified specific EV surface antigens, EV-proteins, and EV microRNAs that can be useful to develop novel diagnostic algorithms to detect, confirm, or follow up the PA. Moreover, the study of EVs in the field of PA provides further insight in the pathophysiological mechanism of the PA disease.
Diagnosis and treatment of primary aldosteronism
Lancet Diabetes Endocrinol 2021 Dec;9(12):876-892.PMID:34798068DOI:10.1016/S2213-8587(21)00210-2.
Primary aldosteronism is a common cause of secondary hypertension associated with excess cardiovascular morbidities. Primary aldosteronism is underdiagnosed because it does not have a specific, easily identifiable feature and clinicians can be poorly aware of the disease. The diagnostic investigation is a multistep process of screening, confirmatory testing, and subtype differentiation of unilateral from bilateral forms for therapeutic management. Adrenal venous sampling is key for reliable subtype identification, but can be bypassed in patients with specific characteristics. For unilateral disease, surgery offers the possibility of cure, with total laparoscopic unilateral adrenalectomy being the treatment of choice. Bilateral forms are treated mainly with mineralocorticoid receptor antagonists. The goals of treatment are to normalise both blood pressure and excessive Aldosterone production, and the primary aims are to reduce associated comorbidities, improve quality of life, and reduce mortality. Prompt diagnosis of primary aldosteronism and the use of targeted treatment strategies mitigate aldosterone-specific target organ damage and with appropriate patient management outcomes can be excellent. Advances in molecular histopathology challenge the traditional concept of primary aldosteronism as a binary disease, caused by either a unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia. Somatic mutations drive autonomous Aldosterone production in most adenomas. Many of these same mutations have been identified in nodular lesions adjacent to an aldosterone-producing adenoma and in patients with bilateral disease. In addition, germline mutations cause rare familial forms of aldosteronism (familial hyperaldosteronism types 1-4). Genetic testing for inherited forms in suspected cases of familial hyperaldosteronism avoids the burdensome diagnostic investigation in positive patients. In this Review, we discuss advances and future management approaches in the diagnosis of primary aldosteronism.
Aldosterone-Producing Adenomas
Vitam Horm 2019;109:407-431.PMID:30678866DOI:10.1016/bs.vh.2018.10.007.
Aldosterone-producing adenomas (APA) are more common than initially anticipated. APA cause primary aldosteronism (PA), which affect 3-10% of the hypertensive population. Research during recent years has led to an increased knowledge of the background dysregulation of the increased Aldosterone release, where mutation in the gene encoding the potassium channel GIRK4-KCNJ5-is the most common. Moreover, the discovery of aldosterone-producing cell clusters in apparently normal adenomas has also led to increased understanding of the development of PA, and presumably also APA. A continuum ranging from low-renin hypertension to APA and overt PA is reasoned, and the secondary effects of Aldosterone on especially the cardiovascular system have also become more evident. Diagnostics of PA and APA is important in order to reduce cardiovascular morbidity and mortality, but the diagnostic methods are somewhat unspecific and insensitive, indicating the need for novel methods.