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Updated: Jul 18, 2026
Primary Culture of Adult Rat Heart Myocytes
Published on: June 16, 2009
Effect of parathyroid hormone on rat heart cells
Insights
High parathyroid hormone (PTH) levels in uremia may damage heart cells by increasing calcium entry and heart rate. This study shows PTH directly affects heart cells, potentially explaining myocardial damage in uremia.
Area of Science:
- Nephrology
- Cardiology
- Endocrinology
Background:
- Uremia is associated with cardiomyopathy, but the underlying mechanisms remain unclear.
- Excessive calcium influx into cardiomyocytes, triggered by catecholamines, can cause myocardial necrosis.
- Elevated parathyroid hormone (PTH) in uremia may contribute to cardiac dysfunction by enhancing calcium entry.
Purpose of the Study:
- To investigate the direct effects of parathyroid hormone (PTH) on cultured rat heart cells.
- To determine if PTH influences cardiomyocyte beating rate, viability, and intracellular signaling pathways.
- To elucidate the role of PTH in potential myocardial damage observed in uremic conditions.
Main Methods:
- Cultured rat heart cells were exposed to various forms of PTH (1-34, 1-84, 53-84) and other agents.
- Measurements included beating rate, cell viability, cyclic AMP production, and responses to calcium modulators.
- Experiments utilized sera from uremic rats with varying parathyroid status.
Main Results:
- Both 1-34 and 1-84 PTH significantly increased cardiomyocyte beating rate and reduced cell survival.
- PTH-induced effects were dose-dependent, reversible upon hormone removal, and dependent on calcium.
- PTH stimulated cyclic AMP production and its action differed from catecholamines, suggesting distinct cellular pathways.
Conclusions:
- Heart cells are a direct target for PTH, with receptors likely present.
- PTH increases heart rate and causes premature cell death, mediated by calcium influx.
- Prolonged exposure to high PTH levels in uremia may lead to myocardial damage, highlighting PTH toxicity.
Abstract:
Myocardiopathy is common in uremia, but its cause in unknown. Excessive entry of calcium in heart cells by catecholamines has been shown to cause necrosis of myocardium. The high blood levels of parathyroid hormone (PTH) in uremia may also enhance entry of calcium into heart cells and exert deleterious effects on the heart. We examined the effect of PTH on rat heart cells grown in culture. Both amino-terminal (1-34) PTH and intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH produced immediate and sustained significant rise in beats per minute and the cells died earlier than control. The effect was reversed if PTH was removed from medium, and was abolished by inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the rise in heart beats, but the effect of 1-84 PTH was significantly greater than that of 1-34 moiety. PTH stimulated cyclic AMP production within 1 min, and cyclic AMP remained significantly elevated thereafter. The effect of PTH required calcium, was mimicked by calcium ionophore, was prevented by verapamil and was not abolished by alpha- or beta-adrenergic blockers. PTH action was additive to phenylephrine and synergistic with isoproterenol. Sera from uremic parathyroidectomized rats did not effect heart beats, but sera from uremic rats with intact parathyroid glands or from uremic-parathyroidectomized rats treated with PTH had effects similar to PTH. Data indicate that (a) heart cell is a target organ for PTH and may have receptors for the hormone; (b) PTH increases beating rate of heart cells and causes early death of cells; (c) PTH effect appears to be due to calcium entry into heart cells; (d) the locus of action through which PTH induces calcium entry is different from that for catecholamines; and (e) uremic serum has no effect unless it contains PTH. Data suggest that myocardial damage may occur in uremia due to prolonged exposure to very high blood levels of PTH, and assign new dimensions to PTH toxicity in uremia.
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