Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Tomaschitz, A; Ritz, E; Pieske, B; Rus-Machan, J; Kienreich, K; Verheyen, N; Gaksch, M; Grübler, M; Fahrleitner-Pammer, A; Mrak, P; Toplak, H; Kraigher-Krainer, E; März, W; Pilz, S.
Aldosterone and parathyroid hormone interactions as mediators of metabolic and cardiovascular disease.
Metabolism. 2014; 63(1):20-31
Doi: 10.1016/j.metabol.2013.08.016
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- Führende Autor*innen der Med Uni Graz
- Tomaschitz Andreas
- Co-Autor*innen der Med Uni Graz
- Fahrleitner-Pammer Astrid
- Grübler Martin
- Keppel Martin Helmut
- Kienreich Katharina
- Kraigher-Krainer Elisabeth
- März Winfried
- Pieske Burkert Mathias
- Pilz Stefan
- Toplak Hermann
- Verheyen Nicolas Dominik
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- Abstract:
- Inappropriate aldosterone and parathyroid hormone (PTH) secretion is strongly linked with development and progression of cardiovascular (CV) disease. Accumulating evidence suggests a bidirectional interplay between parathyroid hormone and aldosterone. This interaction may lead to a disproportionally increased risk of CV damage, metabolic and bone diseases. This review focuses on mechanisms underlying the mutual interplay between aldosterone and PTH as well as their potential impact on CV, metabolic and bone health. PTH stimulates aldosterone secretion by increasing the calcium concentration in the cells of the adrenal zona glomerulosa as a result of binding to the PTH/PTH-rP receptor and indirectly by potentiating angiotensin 2 induced effects. This may explain why after parathyroidectomy lower aldosterone levels are seen in parallel with improved cardiovascular outcomes. Aldosterone mediated effects are inappropriately pronounced in conditions such as chronic heart failure, excess dietary salt intake (relative aldosterone excess) and primary aldosteronism. PTH is increased as a result of (1) the MR (mineralocorticoid receptor) mediated calciuretic and magnesiuretic effects with a trend of hypocalcemia and hypomagnesemia; the resulting secondary hyperparathyroidism causes myocardial fibrosis and disturbed bone metabolism; and (2) direct effects of aldosterone on parathyroid cells via binding to the MR. This adverse sequence is interrupted by mineralocorticoid receptor blockade and adrenalectomy. Hyperaldosteronism due to klotho deficiency results in vascular calcification, which can be mitigated by spironolactone treatment. In view of the documented reciprocal interaction between aldosterone and PTH as well as the potentially ensuing target organ damage, studies are needed to evaluate diagnostic and therapeutic strategies to address this increasingly recognized pathophysiological phenomenon.
- Find related publications in this database (using NLM MeSH Indexing)
- Adrenalectomy - administration & dosage
- Aldosterone - blood, metabolism
- Animals - administration & dosage
- Bone Density - administration & dosage
- Bone Diseases - etiology, metabolism
- Calcium - metabolism
- Cardiovascular Diseases - etiology, metabolism
- Fibrosis - etiology
- Humans - administration & dosage
- Hyperaldosteronism - complications, metabolism
- Hyperparathyroidism, Secondary - complications
- Hypocalcemia - etiology
- Magnesium - metabolism
- Mineralocorticoid Receptor Antagonists - therapeutic use
- Myocardium - pathology
- Parathyroid Hormone - blood, metabolism
- Parathyroidectomy - administration & dosage
- Spironolactone - therapeutic use
- Find related publications in this database (Keywords)
- Aldosterone
- Parathyroid hormone
- Aldosteronism
- Hyperparathyroidism