This TASK-2 underexpression could be attributed to elevated miRNA 23 and 34 levels in ~25% of the APAs and to functional genetic variants in the TASK-2 promoter in another quarter of the cases ( 12), leaving the mechanism for nearly half of the cases unexplained to date.Įlevated serum parathyroid hormone levels have been noted in patients with PA, and type 1 parathyroid hormone receptor has been found in APAs ( 13). Whole transcriptome analysis has demonstrated consistent underexpression of the TASK-2 channels in APAs, and in vitro molecular blunting of TASK-2 enhances aldosterone production ( 12). Study of APAs has been instrumental in recent advances in our understanding of the regulation of normal and pathological aldosterone synthesis. Aldosterone-producing adenomas (APAs) are responsible for about half of PA. Multiple animal models of hyperaldosteronism, including the knockout of TWIK acid–sensitive potassium (TASK) channels types 1 and 3, replicate the PA phenotype in mice ( 11). In the last decade, multiple seminal discoveries have made PA the paradigm of improved mechanistic knowledge in hypertension. In fact, since its discovery in 1954 the term primary has been used to emphasize our ignorance of its causes. PA can mimic primary (essential) hypertension, and is still perceived as an exceptionally rare condition necessitating a complex diagnostic workup, given the lack of known mechanisms and therefore of specific biomarkers. Primary aldosteronism (PA) occurs in 5% to 20% of hypertensive patients ( 9, 10) but is often overlooked because patients are not screened for it. This indicates that aldosterone produced in excess with respect to sodium status is a main determinant of high blood pressure, but it is clear from clinical studies from around the world that inappropriately high aldosterone concentrations produce prominent target organ damage, thus contributing to an ominous prognosis ( 4–8). However, aldosterone levels are inappropriately high in 50% to 80% of all hypertensive disorders, not only primary and secondary aldosteronism but also overweight and obesity ( 1, 2) and the most severe (stage II to III) or drug-resistant forms of hypertension ( 3). The enzyme aldosterone synthase acts in this location.Clinical aspects, such as epidemiology and diagnosis of primary aldosteronism (PA), are briefly reviewed, and the potential role of circulating and tissue biomarkers of APA in subtyping PA is discussedĪldosterone, the main mineralocorticoid hormone, is vital for maintaining body fluid and electrolyte homeostasis, vascular resistance, and, thereby, blood pressure under conditions of salt/water (volume) depletion.
increase water reabsorption through osmosis.Aldosterone regulates the body's concentration of electrolytes, primarily sodium and potassium, by acting on the distal convoluted tubule of kidney nephrons to: In response to increased potassium levels or decreased blood flow to the kidneys, cells of the zona glomerulosa secrete the mineralocorticoid aldosterone into the blood as part of the renin-angiotensin system. Its cells are ovoid in shape and are arranged in clusters or arches ( glomus is Latin for "ball"). The zona glomerulosa of the adrenal gland is the most superficial layer of the adrenal cortex, lying directly beneath the adrenal gland's capsule. List of terms related to Zona glomerulosaĮditor-In-Chief: C. Risk calculators and risk factors for Zona glomerulosaĬauses & Risk Factors for Zona glomerulosa US National Guidelines Clearinghouse on Zona glomerulosaĭirections to Hospitals Treating Zona glomerulosa Ongoing Trials on Zona glomerulosa at Clinical Ĭlinical Trials on Zona glomerulosa at Google Articles on Zona glomerulosa in N Eng J Med, Lancet, BMJĬochrane Collaboration on Zona glomerulosa
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