title: Aldosterone and parathyroid hormone: a precarious couple for cardiovascular disease.
abstract: Animal and human studies support a clinically relevant interaction between aldosterone and parathyroid hormone (PTH) levels and suggest an impact of the interaction on cardiovascular (CV) health. This review focuses on mechanisms behind the bidirectional interactions between aldosterone and PTH and their potential impact on the CV system. There is evidence that PTH increases the secretion of aldosterone from the adrenals directly as well as indirectly by activating the renin-angiotensin system. Upregulation of aldosterone synthesis might contribute to the higher risk of arterial hypertension and of CV damage in patients with primary hyperparathyroidism. Furthermore, parathyroidectomy is followed by decreased blood pressure levels and reduced CV morbidity as well as lower renin and aldosterone levels. In chronic heart failure, the aldosterone activity is inappropriately elevated, causing salt retention; it has been argued that the resulting calcium wasting causes secondary hyperparathyroidism. The ensuing intracellular calcium overload and oxidative stress, caused by PTH and amplified by the relative aldosterone excess, may increase the risk of CV events. In the setting of primary aldosteronism, renal and faecal calcium loss triggers increased PTH secretion which in turn aggravates aldosterone secretion and CV damage. This sequence explains why adrenalectomy and blockade of the mineralocorticoid receptor tend to decrease PTH levels in patients with primary aldosteronism. In view of the reciprocal interaction between aldosterone and PTH and the potentially ensuing CV damage, studies are urgently needed to evaluate diagnostic and therapeutic strategies addressing the interaction between the two hormones.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 15, 8036 Graz, Austria. andreas.tomaschitz@gmx.at
authors.forename: Andreas
authors.initials: A
authors.lastname: Tomaschitz
authors.forename: Eberhard
authors.initials: E
authors.lastname: Ritz
authors.forename: Burkert
authors.initials: B
authors.lastname: Pieske
authors.forename: Astrid
authors.initials: A
authors.lastname: Fahrleitner-Pammer
authors.forename: Katharina
authors.initials: K
authors.lastname: Kienreich
authors.forename: Jörg H
authors.initials: JH
authors.lastname: Horina
authors.forename: Christiane
authors.initials: C
authors.lastname: Drechsler
authors.forename: Winfried
authors.initials: W
authors.lastname: März
authors.forename: Michael
authors.initials: M
authors.lastname: Ofner
authors.forename: Thomas R
authors.initials: TR
authors.lastname: Pieber
authors.forename: Stefan
authors.initials: S
authors.lastname: Pilz
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D002908:Chronic Disease; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology; D006439:Hemodynamics; D006801:Humans; D006929:Hyperaldosteronism / Q000378:metabolism / Q000503:physiopathology; D049950:Hyperparathyroidism, Primary / Q000378:metabolism / Q000503:physiopathology; D010281:Parathyroid Hormone / Q000378:metabolism*; D012084:Renin-Angiotensin System; D015398:Signal Transduction
chemical_list: D010281:Parathyroid Hormone; D000450:Aldosterone