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First Publication for EU-MASCARA
Monday, Feb 13, 2012
Tomaschitz A, Ritz E, Pieske B, Fahrleitner-Pammer A, Kienreich K, Horina JH, Drechsler C, März W, Ofner M, Pieber TR, Pilz S.

Cardiovasc Res . 2012 Apr 1;94(1):10-9. Epub 2012 Feb 13.

Summary:
Accumulating evidence suggests that bidirectional interactions between aldosterone and parathyroid hormone have potential effects on the cardiovascular system. Activation of both the PTH/PTH-RP receptor and voltage-gated L-type calcium channels mediate PTH-dependent calcium entry in zona glomerulosa cells resulting in an enhanced aldosterone synthesis. This is in line with significantly decreased circulating aldosterone levels followed by parathyroidectomy in patients suffering from primary hyperparathyroidism. In animal models of heart failure relative aldosterone excess induces a pronounced renal calcium loss, which in turn activates the parathyroid Ca-sensing receptors and aggravates secondary hyperparathyroidism. In patients with chronic heart failure elevated PTH levels stimulate both aldosterone synthesis and bone resorption, which results in a higher fracture risk within this patient group. Compared with essential hypertensives patients subjects with primary aldosteronism have higher PTH levels that are significantly reduced after either MR-blockade treatment or adrenalectomy. In summary, the identification of a specific bidirectional interaction between aldosterone and PTH represent a novel mechanism for aldosterone and PTH mediated cardiovascular damage

[PubMed: http://www.ncbi.nlm.nih.gov/pubmed/22334595]