Calcium channel involvement in potassium depolarization-induced phosphoinositide hydrolysis in rat cortical slices.

Neurochemical Research
R A Gonzales, L D Minor

Abstract

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 inhibit...Continue Reading

References

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Citations

May 26, 1995·European Journal of Pharmacology·M MosaddeghiD Paul
Nov 1, 1993·Journal of Cerebral Blood Flow and Metabolism : Official Journal of the International Society of Cerebral Blood Flow and Metabolism·S L CohanP Cyr

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