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Muscarinic receptor antagonist effects in parotid acini and M1-CHO cells: evidence of G protein involvement
V J Horn1, B J Baum, I S Ambudkar
1Clinical Investigations and Patient Care Branch, National Institute of Dental Research, National Institutes of Health, Bethesda, MD 20892.
Abstract:
We have examined the effects of the muscarinic antagonist atropine, on non-receptor-mediated activation of intracellular calcium (Ca2+i) mobilization events. In dispersed rat parotid acini, atropine significantly lowered basal inositol trisphosphate levels and delayed AlF4(-)-stimulated Ca2+i elevation in a dose-dependent manner. In a cell line transfected with the m1 muscarinic receptor (M1-CHO), atropine significantly lowered (approximately 60%) AlF4- stimulated Ca2+i elevation. These aggregate findings suggest that atropine, acting via the muscarinic receptor, decreases the efficacy of G protein-mediated activation of phospholipase C.
Insights
Atropine, a muscarinic antagonist, reduces intracellular calcium mobilization by inhibiting G protein-mediated phospholipase C activation. This effect was observed in rat parotid acini and M1-CHO cells, indicating atropine
Area of Science:
- Pharmacology
- Cell Biology
- Biochemistry
Background:
- Muscarinic antagonists like atropine are widely used.
- Intracellular calcium (Ca2+i) mobilization is crucial for cellular signaling.
- The role of atropine in non-receptor-mediated Ca2+i events requires further elucidation.
Purpose of the Study:
- To investigate the effects of atropine on non-receptor-mediated intracellular calcium mobilization.
- To determine if atropine influences basal inositol trisphosphate levels.
- To assess atropine's impact on G protein-mediated activation of phospholipase C.
Main Methods:
- Experiments were conducted using dispersed rat parotid acini.
- A cell line transfected with the m1 muscarinic receptor (M1-CHO) was utilized.
- Measurements included basal inositol trisphosphate levels and AlF4(-)-stimulated Ca2+i elevation.
Main Results:
- Atropine significantly reduced basal inositol trisphosphate levels in rat parotid acini.
- Atropine dose-dependently delayed AlF4(-)-stimulated Ca2+i elevation in rat parotid acini.
- Atropine significantly lowered AlF4(-)-stimulated Ca2+i elevation in M1-CHO cells by approximately 60%.
Conclusions:
- Atropine, acting through muscarinic receptors, decreases the efficacy of G protein-mediated phospholipase C activation.
- These findings highlight a non-receptor-mediated effect of atropine on calcium signaling pathways.
- Atropine's influence extends beyond its known receptor interactions, impacting fundamental cellular signaling mechanisms.