Pharmacological treatment of aldosterone excess

Deinum, Jaap; Riksen, Niels P.; Lenders, Jacques W.M.

doi:10.1016/j.pharmthera.2015.07.006

Cited by 34 publications

(32 citation statements)

References 177 publications

(198 reference statements)

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“…En los casos de HP bilateral (adenoma bilateral, hiperplasia adrenal bilateral, hiperaldosteronismo familiar) o en casos donde no es posible el tratamiento quirúrgico, se recomienda el tratamiento médico con antagonistas de los receptores mineralocorticoides: la espironolactona como primera opción y la eplenona como alternativa (1,8,11) .…”

Section: Las Guías De Launclassified

Hypertension secondary to primary hyperaldosteronism

González

Bogado

Arrieta

2019

Rev. Nac. (Itauguá)

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La hipertensión arterial es una afección pandémica responsable de varias complicaciones cardiovasculares, neurológicas y renales. La gran mayoría se debe a la hipertensión esencial o primaria, pero cada vez se diagnostican más casos de hipertensión arterial secundaria, ya sea de causa endocrinológica, renal o neurológica. Se presenta un caso de hipertensión secundaria a hiperaldosteronismo primario.

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Section: Las Guías De Launclassified

Hypertension secondary to primary hyperaldosteronism

González

Bogado

Arrieta

2019

Rev. Nac. (Itauguá)

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“…Its better tolerability profile needs to be balanced against its higher cost and the possibility that spironolactone may lower BP more effectively than eplerenone in the medical treatment of PA [1]. Eplerenone is a good alternative in case of side effects of spironolactone [66].…”

Section: Eplerenonementioning

confidence: 99%

Update in diagnosis and management of primary aldosteronism

Dick

Queiroz

Bernardi

et al. 2017

Clinical Chemistry and Laboratory Medicine (CCLM)

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Primary aldosteronism (PA) is a group of disorders in which aldosterone is excessively produced. These disorders can lead to hypertension, hypokalemia, hypervolemia and metabolic alkalosis. The prevalence of PA ranges from 5% to 12% around the globe, and the most common causes are adrenal adenoma and adrenal hyperplasia. The importance of PA recognition arises from the fact that it can have a remarkably adverse cardiovascular and renal impact, which can even result in death. The aldosterone-to-renin ratio (ARR) is the election test for screening PA, and one of the confirmatory tests, such as oral sodium loading (OSL) or saline infusion test (SIT), is in general necessary to confirm the diagnosis. The distinction between adrenal hyperplasia (AH) or aldosteroneproducing adenoma (APA) is essential to select the appropriate treatment. Therefore, in order to identify the subtype of PA, imaging exams such as computed tomography or magnetic ressonance imaging, and/or invasive investigation such as adrenal catheterization must be performed. According to the subtype of PA, optimal treatment -surgical for APA or pharmacological for AH, with drugs like spironolactone and amiloride -must be offered.

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“…The mineralocorticoid hormone aldosterone is the most distal element of the renin angiotensin aldosterone system (RAAS) and regulates water and electrolyte balance [1,2]. The most proximal component of the RAAS, renin, is secreted in response to low sodium intake or decreased blood pressure and converts angiotensinogen into angiotensin I. Angiotensin converting enzyme (ACE) then generates Ang II that binds to angiotensin II receptors type 1 (AT 1 ) and 2 (AT 2 ), including in the adrenal gland, where it stimulates aldosterone secretion.…”

Section: Introductionmentioning

confidence: 99%

“…The most proximal component of the RAAS, renin, is secreted in response to low sodium intake or decreased blood pressure and converts angiotensinogen into angiotensin I. Angiotensin converting enzyme (ACE) then generates Ang II that binds to angiotensin II receptors type 1 (AT 1 ) and 2 (AT 2 ), including in the adrenal gland, where it stimulates aldosterone secretion. Aldosterone production is also regulated by potassium and adrenocorticotropic hormone (ACTH) [1]. Excessive Ang II and aldosterone actions are involved in the pathogenesis of atherosclerosis, hypertension, obesity, and type 2 diabetes [3].…”

Section: Introductionmentioning

confidence: 99%

“…Aldosterone is generated by the aldosterone synthase enzyme (CYP11B2) in the zona glomerulosa of the adrenal cortex. CYP11B2 catalyzes the 3 step conversion of 11-deoxycorticosterone to aldosterone via the intermediates corticosterone, and 18-OH-corticosterone [1,2]. In the zona fasciculata of the adrenal cortex, the 93 % identical CYP11B1 (steroid-11β-hydroxylase, cortisol synthase) catalyzes the synthesis of the glucocorticoid cortisol from 11-deoxycortisol [2].…”

Section: Introductionmentioning

confidence: 99%

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Impact of Aldosterone Synthase Inhibitor FAD286 on Steroid Hormone Profile in Human Adrenocortical Cells

et al. 2017

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Inhibition of aldosterone synthase (CYP11B2) is an alternative treatment option to mineralocorticoid receptor antagonism to prevent harmful aldosterone effects. FAD286 is the best characterized aldosterone synthase inhibitor. However, to date, no study has used sensitive liquid chromatography-tandem mass spectrometry to characterize in detail the effect of FAD286 on the secreted steroid hormone profile of adrenocortical cells. Basal aldosterone production in NCI-H295R cells was detectable and 9-fold elevated after stimulation with angiotensin II. FAD286 inhibited this increase, showing a maximal effect at 10 nmol/l. Higher concentrations of FAD286 did not further reduce aldosterone concentrations, but showed a parallel reduction in corticosterone, cortisol and cortisone levels, reflecting additional inhibition of steroid-11β-hydroxylase (CYP11B1). Pregnenolone, progesterone and 17-OH-progesterone levels remained unaffected. In conclusion, the aldosterone synthase inhibitor FAD286 lowers angiotensin II-induced aldosterone concentrations in adrenocortical cells but the relative lack of selectivity over CYP11B1 is evident at higher FAD286 concentrations.

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Pharmacological treatment of aldosterone excess

Cited by 34 publications

References 177 publications

Hypertension secondary to primary hyperaldosteronism

Hypertension secondary to primary hyperaldosteronism

Update in diagnosis and management of primary aldosteronism

Impact of Aldosterone Synthase Inhibitor FAD286 on Steroid Hormone Profile in Human Adrenocortical Cells

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