Calcium channel involvement in potassium depolarization-induced phosphoinositide hydrolysis in rat cortical slices
Autor: | Lerna D. Minor, Rueben A. Gonzales |
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Rok vydání: | 1989 |
Předmět: |
Male
medicine.medical_specialty medicine.drug_class chemistry.chemical_element Calcium channel blocker Calcium In Vitro Techniques Phosphatidylinositols Biochemistry Cellular and Molecular Neuroscience chemistry.chemical_compound Nitrendipine Internal medicine medicine Animals Inositol Inositol phosphate chemistry.chemical_classification Cerebral Cortex Calcium channel Dihydropyridine Inositol trisphosphate Rats Inbred Strains General Medicine 3-Pyridinecarboxylic acid 1 4-dihydro-2 6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)- Methyl ester Rats Endocrinology chemistry Potassium Calcium Channels medicine.drug |
Zdroj: | Neurochemical research. 14(11) |
ISSN: | 0364-3190 |
Popis: | The stimulation of production of inositol phosphates in rat cortical slices by KCl depolarization and the effects of calcium channel active drugs were investigated. Elevation of K+ in the medium up to 48 mM KCl caused a linear concentration-dependent increase in [3H]inositol phosphate accumulation. The KCl stimulated response was not significantly inhibited in the presence of muscarinic or alpha 1-adrenergic antagonists. KCl stimulated the production of inositol trisphosphate at 60 min but not 10 min. Addition of peptidase inhibitors did not significantly affect KCl-stimulated PI hydrolysis. The KCl-stimulated response was still observed in the absence of extracellular calcium, although the net accumulation of inositol phosphates was greater in the presence of 0.1 or 0.5 mM calcium. KCl (48 mM) inhibited [3H]inositol uptake into phospholipids of cortical slices. The dihydropyridine calcium channel agonist BAY K 8644 stimulated PI hydrolysis in cortical slices in a concentration dependent manner in the presence of 19 mM KCl. The BAY K 8644-stimulated PI response was partially inhibited by 1 microM atropine but not by 1 microM prazosin. Calcium channel blockers nitrendipine, verapamil, flunarizine, and nifedipine slightly inhibited the PI response stimulated by 19 mM KCl in the presence or absence of BAY K 8644. The effects of the calcium channel antagonists were attenuated in the presence of 1 microM atropine. The peptide calcium channel blocker omega-conotoxin did not affect KCl-stimulated PI hydrolysis. These results suggest that endogenous muscarinic or adrenergic neurotransmitters are not involved in KCl-stimulated PI hydrolysis in cortical slices. Although extracellular calcium is necessary for optimal KCl-stimulated PI hydrolysis, it is not required for the expression of the KCl-evoked response suggesting that depolarization is the primary trigger for this stimulant. |
Databáze: | OpenAIRE |
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