Journal
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY AND THERAPEUTICS
Volume 14, Issue 3, Pages 242-247Publisher
SAGE PUBLICATIONS INC
DOI: 10.1177/1074248409339308
Keywords
animal models; arrhythmias; Ca2+; M-3-mAChR; pilocarpine
Funding
- National Basic Research program of China [200703 512000, 2007CB 512006]
- National Natural Science Foundation of China [30672462]
- Heilongjiang Postdoctoral Sustentation Fund, China
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This study was designed to evaluate the effects of pilocarpine and explore the underlying ionic mechanism, using both aconitine-induced rat and ouabain-induced guinea pig arrhythmia models. Confocal microscopy was used to measure intracellular free-calcium concentrations ([Ca2+](i)) in isolated myocytes. The Current data showed that pilocarpine significantly delayed onset of arrhythmias, decreased the time course of ventricular tachycardia and fibrillation, reduced arrhythmia score, and increased the survival time of arrhythmic rats and guinea pigs. [Ca2+](i) overload induced by aconitine or ouabain was reduced in isolated myocytes pretreated with pilocarpine. Moreover, M-3-muscarinic acetylcholine receptor (mAChR) antagonist 4-DAMP (4-diphenylacetoxy-N-methylpiperidine-methiodide) partially abolished the beneficial effects of pilocarpine. These data suggest that pilocarpine produced antiarrhythmic actions on arrhythmic rat and guinea pig models induced by aconitine or ouabain via stimulating the cardiac M-3-mAChR. The mechanism may be related to the improvement of Ca2+ handling.
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