Primary hyperaldosteronism. Mechanisms and consequences of pathological influence on an organism (review of literature)

Main Article Content

V.А. Shidlovsky
А.V. Shidlovsky
V.V. Kravtsiv


The work is based on the analysis of world literature data on primary hyperaldosteronism. The data on mechanisms of pathological influences of excessive autonomous aldosterone secretion on the body systems are given. The ways of excessive aldosterone influence on the cardiovascular and nervous system, kidneys, quality and life expectancy are revealed. It is shown that aldosterone activates specific intracellular genomic and non-genomic pathways of influence on the cardiovascular system and induces the development of cardiofibrosis, atrial fibrillation and heart failure. Attention is drawn to the fact that hyperaldostero­nism is a cause of the development of metabolic syndrome, deterioration in quality of life and reduction of life expectancy.

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How to Cite
Shidlovsky, V., Shidlovsky А., and V. Kravtsiv. “Primary Hyperaldosteronism. Mechanisms and Consequences of Pathological Influence on an Organism (review of Literature)”. INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), vol. 15, no. 4, Feb. 2019, pp. 351-7, doi:10.22141/2224-0721.15.4.2019.174824.
To practicing Endocrinologists


Pishak VP, Krivchanska MI. Renin-angiotensin-aldosterone system: molecular mechanism of regulation and polymorphism of genes in pathology. Biological systems. 2013;5(3):305-310. (In Ukrainian).

Korolyuk OYa, Radchenko OM. The role of the renin-angiotensin-aldosterone system in the regulation of blood pressure: a review of literature. Medical Newspaper Health of Ukraine 21st Century. 2018;20(441):12-13. (in Ukrainian).

Mondaca-Ruff D, Riquelme JA, Quiroga C, et al. Angiotensin II-Regulated Autophagy Is Required for Vascular Smooth Muscle Cell Hypertrophy. Front Pharmacol. 2019 Feb 5;9:1553. doi: 10.3389/fphar.2018.01553.

Mentz RJ, Bakris GL, Waeber B, et al. The past, present and future of renin-angiotensin aldosterone system inhibition. Int J Cardiol. 2013 Sep 1;167(5):1677-87. doi: 10.1016/j.ijcard.2012.10.007.

Touyz RM, Alves-Lopes R, Rios FJ, et al. Vascular smooth muscle contraction in hypertension. Cardiovascular Research. 2018;114(4):529-539. doi: 10.1093/cvr/cvy023.

Antoniak S, Cardenas JC, Buczek LJ, Church FC, Mackman N, Pawlinski R. Protease-Activated Receptor 1 Contributes to Angiotensin II-Induced Cardiovascular Remodeling and Inflammation. Cardiology. 2017;136(4):258-268. doi: 10.1159/000452269.

Dell’Italia LJ. Translational success stories: angiotensin receptor 1 antagonists in heart failure. Circ Res. 2015 Jan 2;116(1):206-13. doi: 10.1161/CIRCRESAHA.116.302706.

Bollag WB. Regulation of aldosterone synthesis and secretion. Compr Physiol. 2014 Jul;4(3):1017-55. doi: 10.1002/cphy.c130037.

Baker ME, Katsu Y. 30 YEARS OF THE MINERALOCORTICOID RECEPTOR: Evolution of the mineralocorticoid receptor: Sequence, structure and function J Endocrinol. 2017 Jul;234(1):T1-T16. doi: 10.1530/JOE-16-0661.

Wynne BM, Chiao CW, Webb RC. Vascular Smooth Muscle Cell Signaling Mechanisms for Contraction to Angiotensin II and Endothelin-1. J Am Soc Hypertens. 2009 Mar-Apr;3(2):84-95. doi: 10.1016/j.jash.2008.09.002.

Buggey J, Mentz RJ, Pitt B, et al. A reappraisal of loop diuretic choice in heart failure patients. Am Heart J. 2015 Mar;169(3):323-33. doi: 10.1016/j.ahj.2014.12.009.

Grossmann C, Gekle M. Non-classical actions of the mineralocorticoid receptor: misuse of EGF receptors? Mol Cell Endocrinol. 2007 Oct 15;277(1-2):6-12. doi: 10.1016/j.mce.2007.07.001.

Connell JMC, Davies E. The new biology of aldosterone. J Endocrinol. 2005 Jul;186(1):1-20. doi: 10.1677/joe.1.06017.

Welling PA. Regulation of renal potassium secretion: molecular mechanisms. Semin Nephrol. 2013 May;33(3):215-28. doi: 10.1016/j.semnephrol.2013.04.002.

Kamel KS, Schreiber M, Halperin ML. Renal potassium physiology: integration of the renal response to dietary potassium depletion. Kidney Int. 2018 Jan;93(1):41-53. doi: 10.1016/j.kint.2017.08.018.

Stowasser M, Gordon RD. Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney. Physiol Rev. 2016 Oct;96(4):1327-84. doi: 10.1152/physrev.00026.2015.

Davel AP, Jaffe IZ, Tostes RC, Jaisser F, Belin de Chantemèle EJ. New roles of aldosterone and mineralocorticoid receptors in cardiovascular disease: translational and sex-specific effects. Am J Physiol Heart Circ Physiol. 2018 Oct 1;315(4):H989-H999. doi: 10.1152/ajpheart.00073.2018.

Sahay M, Sahay RK. Low renin hypertension. Indian J Endocrinol Metab. 2012 Sep;16(5):728-39. doi: 10.4103/2230-8210.100665.

Baudrand R, Vaidya A. The Low-Renin Hypertension Phenotype: Genetics and the Role of the Mineralocorticoid Receptor. Int J Mol Sci. 2018 Feb 11;19(2). pii: E546. doi: 10.3390/ijms19020546.

Stowasser M, Gordon RD. Primary Aldosteronism: Changing Definitions and New Concepts of Physiology and Pathophysiology Both Inside and Outside the Kidney. Physiol Rev. 2016 Oct;96(4):1327-84. doi: 10.1152/physrev.00026.2015.

López B, González A, Ravassa S, et al. Circulating Biomarkers of Myocardial Fibrosis: The Need for a Reappraisal. J Am Coll Cardiol. 2015 Jun 9;65(22):2449-56. doi: 10.1016/j.jacc.2015.04.026.

Ho JE, Shi L, Day SM, Colan SD, Russell MW, Towbin JA, Sherrid MV. Biomarkers of cardiovascular strees and fibrosis in preclinical hypertrophic cardiomyopathy. Open Heart. 2017 Nov 1;4(2):e000615. doi: 10.1136/openhrt-2017-000615.

Lim JS, Park S, Park SI, et al. Cardiac Dysfunction in Association with Increased Inflammatory Markers in Primary Aldosteronism. Endocrinol Metab (Seoul). 2016 Dec;31(4):567-576. doi: 10.3803/EnM.2016.31.4.567.

Cannavo A, Bencivenga L, Liccardo D. Aldosterone and Mineralocorticoid Receptor System in Cardiovascular Physiology and Pathophysiology. Oxid Med Cell Longev. 2018 Sep 19;2018:1204598. doi: 10.1155/2018/1204598.

Chen ZW, Hung CS, Wu VC, Lin YH. Primary Aldosteronism and Cerebrovascular Diseases. Endocrinol Metab (Seoul). 2018 Dec;33(4):429-434. doi: 10.3803/EnM.2018.33.4.429.

Young WF. Pathophysiology and clinical features of primary aldosteronism. 2018. Available from:

Hundemer GL, Curhan GC, Yozamp N, Wang M, Vaidya A. Incidence of Atrial Fibrillation and Mineralocorticoid Receptor Activity in Patients With Medically and Surgically Treated Primary Aldosteronism. JAMA Cardiol. 2018 Aug 1;3(8):768-774. doi: 10.1001/jamacardio.2018.2003.

Stowasser M, Sharman J, Leano R, Gordon RD, Ward G, Cowley D, Marwick TH. Evidence for abnormal left ventricular structure and function in normotensive individuals with familial hyperaldosteronism type I. J Clin Endocrinol Metab. 2005 Sep;90(9):5070-5076. doi: 10.1210/jc.2005-0681.

Stein DL, Yee J. Dr. Conn Lives on: Insights Into Screening and Genetics of Primary Aldosteronism. Adv Chronic Kidney Dis. 2019 Mar;26(2):81-84. doi: 10.1053/j.ackd.2019.03.018.

Borst O, Schmidt EM, Munzer P, et al. The serum- and glucocorticoid-inducible kinase 1 (SGK1) influences platelet calcium signaling and function by regulation of Orai1 expression in megakaryocytes. Blood. 2012 Jan 5;119(1):251-61. doi: 10.1182/blood-2011-06-359976.

Tang L, Li X, Wang B, et al. Clinical Characteristics of Aldosterone- and Cortisol-Coproducing Adrenal Adenoma in Primary Aldosteronism. Int J Endocrinol. 2018 Mar 25;2018:4920841. doi: 10.1155/2018/4920841.

Nykonenko AO, Zubryk IV, Podluzhnyi OO, Yakymenko VV. Аnalysis of the renal hemodynamics state in patients, suffering primary hyperaldosteronism in accordance to data of ultrasonographic Doppler scanning. Klinicheskaia Khirurgiia. 2019;86(1):35-39. doi: 10.26779/2522-1396.2019.01.35.

Kramers BJ, Kramers C, Lenders JW, Deinum J. Effects of Treating Primary Aldosteronism on Renal Function. J Clin Hypertens (Greenwich). 2017 Mar;19(3):290-295. doi: 10.1111/jch.12914.

Hanslik G, Wallaschofski H, Dietz A, et al. Increased prevalence of diabetes mellitus and the metabolic syndrome in patients with primary aldosteronism of the German Conn's Registry. Eur J Endocrinol. 2015 Nov;173(5):665-75. doi: 10.1530/EJE-15-0450.

Fallo F, Veglio F, Bertello C, et al. Prevalence and characteristics of the metabolic syndrome in primary aldosteronism. J Clin Endocrinol Metab. 2006 Feb;91(2):454-9. doi: 10.1210/jc.2005-1733.

Fallo F, Della Mea P, Sonino N, et al. Adiponectin and insulin sensitivity in primary aldosteronism. Am J Hypertens. 2007 Aug;20(8):855-61. doi: 10.1016/j.amjhyper.2007.03.012.

Iacobellis G, Petramala L, Cotesta D, et al. Adipokines and Cardiometabolic Profile in Primary Hyperaldosteronism. J Clin Endocrinol Metab. 2010 May;95(5):2391-8. doi: 10.1210/jc.2009-2204.

Iacobellis G, Petramala L, Cotesta D, et al. Adipokines and Cardiometabolic Profile in Primary Hyperaldosteronism. J Clin Endocrinol Metab. 2010 May;95(5):2391-8. doi: 10.1210/jc.2009-2204.

Monticone S, Burrello J, Tizzan D, Bertello C, Viola A, Buffolo F. Prevalence and Clinical Manifestations of Primary Aldosteronism Encountered in Primary Care Practic. J Am Coll Cardiol. 2017 Apr 11;69(14):1811-1820. doi: 10.1016/j.jacc.2017.01.052.

Apostolopoulou K, Kunzel HE, Gerum S, et al. Gender differences in anxiety and depressive symptoms in patients with primary hyperaldosteronism: across-sectional study. World J Biol Psychiatry. 2014 Jan;15(1):26-35. doi: 10.3109/15622975.2012.665480.

Indra T, Holaj R, Štrauch B, et al. Long-term effects of adrenalectomy or spironolactone on blood pressure control and regression of left ventricle hypertrophy in patients with primary aldosteronism. J Renin Angiotensin Aldosterone Syst. 2015 Dec;16(4):1109-17. doi: 10.1177/1470320314549220.

Briet M, Schiffrin EL. Vascular Actions of Aldosterone. J Vasc Res. 2013;50(2):89-99. doi: 10.1159/000345243.

Catena C, Colussi G, Nadalini E, et al. Cardiovascular outcomes in patients with primary aldosteronism after treatment. Arch Intern Med. 2008 Jan 14;168(1):80-5. doi: 10.1001/archinternmed.2007.33.

Tuka V, Matoulek M, Rosa J, et al. The Effect of Adrenalectomy on Exercise Response of the ReninAngiotensin-Aldosterone System and Exercise Tolerance in Primary Aldosteronism. Physiol Res. 2018 May 4;67(2):233-238. doi: 10.33549/physiolres.933651.