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Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Digoxin-associated decrease in parathyroid hormone (PTH) concentrations in patients with atrial fibrillation.
Arie Apel1, Pauzner Rachel, Ohad Cohen
1Department of Medicine E, Chaim Sheba Medical Center, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel
European Journal of Clinical Investigation
|December 18, 2012
Summary
Digoxin treatment decreased parathyroid hormone (PTH) levels in patients with atrial fibrillation, suggesting the sodium pump
Area of Science:
- Endocrinology
- Calcium Homeostasis
- Pharmacology
Background:
- Parathyroid hormone (PTH) secretion is primarily regulated by the calcium-sensing receptor.
- Klotho influences PTH secretion by recruiting Na-K-ATPase and modulating FGF23 effects.
- Ouabain, a Na-K-ATPase inhibitor, prevents PTH increase in hypocalcemia, suggesting a role for the sodium pump.
Purpose of the Study:
- To investigate the effect of digoxin, a Na-K-ATPase modulator, on parathyroid hormone (PTH) levels in humans.
- To explore the potential role of the sodium pump in human PTH homeostasis.
Main Methods:
- Twenty patients with atrial fibrillation were divided into two groups: digoxin (n=10) and verapamil (n=10).
- 0.25 mg digoxin was administered, and plasma PTH, ionized calcium, and digoxin levels were measured at intervals up to 4 hours.
- Verapamil served as a control.
Main Results:
- Plasma PTH concentrations decreased in the digoxin group, while they increased in the control group.
- Ionized calcium levels remained stable in both groups throughout the study.
- A blunting of the morning circadian rhythm of PTH levels was observed.
Conclusions:
- Digoxin treatment led to a decrease in plasma PTH concentrations in normocalcemic patients.
- The sodium pump appears to play a significant role in human PTH secretion and calcium homeostasis.
- Targeting the sodium pump may offer a novel therapeutic approach for calcium regulatory disorders.
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