Abstract
The effects of melatonin treatment on cardiac sarcolemmal membrane function were investigated in alloxan-injected rats. Ca2+-stimulated adenosinetriphosphatase (ATPase, Ca2+ pump) and Mg2+-ATPase activities were depressed significantly in sarcolemmal preparations from alloxan- injected rats compared with levels in control rats. These deficits were observed 2 days after alloxan injection, and they were accompanied by an increase in the density of voltage-sensitive calcium channels, as measured by the [3H]nitrendipine-binding assay. In a dose-dependent manner, treatment of rats with melatonin before alloxan injection significantly overcame the suppression of Ca2+-stimulated ATPase in cardiac sarcolemma. Melatonin (1, 5, and 10 mg/kg) overcame Ca2+-stimulated ATPase suppression by 13, 35, and 70%, respectively. In addition, melatonin at a dose of 10 mg/kg also prevented the suppression of the Mg2+-ATPase by 31%. The number of [3H]nitrendipine-binding sites was not influenced by melatonin. The patent Na+-K+-ATPase and ouabain-sensitive Na+-K+-ATPase activities were not different between the control and experimental groups. The results indicate that Ca2+ pump activity is suppressed by acute alloxan treatment, whereas the density of voltage-sensitive calcium channels is increased. These changes may be a consequence of alloxan toxicity to the cardiac sarcolemma. Melatonin, likely because of its antioxidant capacity, exerts a protective effect on heart sarcolemmal membrane function in alloxan-injected rats.
Original language | English (US) |
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Pages (from-to) | E57-E62 |
Journal | American Journal of Physiology - Endocrinology and Metabolism |
Volume | 267 |
Issue number | 1 30-1 |
DOIs | |
State | Published - 1994 |
Keywords
- [H]nitrendipine
- alloxan
- calcium channel
- calcium ion-stimulated adenosinetriphosphatase
- heart sarcolemma
- magnesium ion- adenosinetriphosphatase
- melatonin
- sodium-potassium-adenosinetriphosphatase
ASJC Scopus subject areas
- General Medicine