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Sarcoplasmic reticulum Ca2+ transport and long chain acylcarnitines in hyperthyroidism
S C Black1, J H McNeill, S Katz
1Division of Pharmacology and Toxicology, Faculty of Pharmaceutical Sciences, University of British Columbia, Vancouver, Canada.
Canadian Journal of Physiology and Pharmacology
|February 1, 1988
Summary
Thyroid hormone (T3) treatment significantly enhances cardiac sarcoplasmic reticulum calcium transport in rats. This improvement correlates with reduced long-chain acylcarnitine levels in the SR membrane.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Molecular Biology
Background:
- Thyroid hormones play a crucial role in regulating cardiac function.
- Hyperthyroidism can lead to significant alterations in myocardial contractility and relaxation.
- Cardiac sarcoplasmic reticulum (SR) is vital for regulating intracellular calcium levels during muscle contraction and relaxation.
Purpose of the Study:
- To investigate the effects of L-3,5,3'-triiodothyronine (T3) on cardiac sarcoplasmic reticulum (SR) calcium transport.
- To determine the relationship between T3-induced changes in SR calcium transport and carnitine derivative levels.
Main Methods:
- Male Wistar rats were administered L-3,5,3'-triiodothyronine (T3).
- Cardiac SR was isolated at various time points post-treatment.
- Calcium transport activity and levels of carnitine derivatives (total carnitine, long-chain acylcarnitine) were measured.
Main Results:
- T3 treatment significantly augmented SR calcium transport at all tested calcium concentrations.
- Calcium-dependent phosphoprotein levels in SR increased at 48 and 72 hours.
- Total SR carnitine and long-chain acylcarnitine (LCAC) levels were reduced following T3 administration.
Conclusions:
- T3-induced hyperthyroidism enhances cardiac SR calcium transport.
- The augmented calcium transport may be associated with a reduction in endogenous long-chain acylcarnitine levels within the SR membrane.