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Cardiovascular Research Advance Access first published online on January 24, 2009
This version [Corrected Proof] published online on February 17, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp027
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Parathyroid hormone improves contractile performance of adult rat ventricular cardiomyocytes at low concentrations in a non-acute way

Ilhan Tastan, Rolf Schreckenberg, Solaiman Mufti, Yaser Abdallah, Hans Michael Piper and Klaus-Dieter Schlüter*

Justus-Liebig-Universität Giessen, Physiologisches Institut, Aulweg 129, D-35392 Giessen, Germany

* Corresponding author. Tel: +49 641 99 47 212; fax: +49 641 99 47 219. E-mail address: klaus-dieter.schlueter{at}physiologie.med.uni-giessen.de

Aims: In patients with congestive heart failure, plasma parathyroid hormone (PTH) levels are positively associated with cardiac function. PTH, used to mobilize stem cells from the bone marrow after myocardial infarction, causes an increased left ventricular ejection fraction. The aim of this study was to investigate whether low but plasma-relevant concentrations of PTH directly influence the contractile properties of cardiomyocytes.

Methods and results: Isolated adult rat ventricular cardiomyocytes were exposed to PTH(1–34) or full-length PTH at picomolar concentrations for 24 h. Cell shortening was measured at 2 Hz as a cellular correlate of inotropic responsiveness. Intracellular calcium was measured in Fura-AM-loaded cells. PTH(1–3) (20–200 pM) and full-length PTH (200 pM) increased cell shortening within 24 h. PTH had no effect on cell size, but resting and peak systolic calcium concentrations were elevated. The beneficial effect of PTH was mediated via its cAMP/protein kinase A-activating domain and attenuated by addition of a protein kinase A inhibitor. In contrast, PTH peptides representing a protein kinase C-activating domain but not a cAMP/protein kinase A-activating domain or peptides that represent none of these domains had no effect on cell shortening. The effect of PTH on cell shortening was strong at low concentrations of extracellular calcium but declined at higher calcium concentrations. PTH downregulated the expression of the calcium sensing receptor, a receptor known to antagonize the action of PTH on calcium transport. Furthermore, PTH antagonized the angiotensin II-induced loss of cell function.

Conclusion: Low concentrations of PTH improve cell shortening by increasing calcium load at rest. By this mechanism cardiomyocytes compensate reduced extracellular calcium levels as they occur in patients with heart failure.

KEYWORDS Heart function; Calcium sensing receptor; Inotropy

Time for primary review: 42 days

This paper was guest edited by Håvard Attramdal, University of Oslo, Norway.


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