Abstract
It has been reported that cis-unsaturated free fatty acids (cis-FFA) block intracellular Ca2+ rise in EGFR T17 and GH3 cells by perturbing the generation of Ins(1,4,5)P3. In the present work, it was found that cis-FFA did not alter potassium-induced cell depolarization in GH3 cells, while blocking Ca2+ rise and GH secretion. Interestingly enough, saturated or trans-unsaturated FFA exert the opposite actions, i.e., they block cell depolarization without altering Ca2+ rise and hormone secretion. As depolarization activates GH3 cells via direct opening of Ca2+ channels with no generation of intracellular mediators, these results suggest that cis-FFA act by a direct perturbation of the Ca2+ channel opening.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Calcium / metabolism*
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Calcium Channels / chemistry
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Calcium Channels / drug effects
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Calcium Channels / physiology*
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Cells, Cultured
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Ethanol / pharmacology
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Fatty Acids, Nonesterified / pharmacology*
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Fatty Acids, Unsaturated / pharmacology*
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Gramicidin / pharmacology
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Growth Hormone / metabolism*
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Kinetics
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Membrane Potentials / drug effects
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Nimodipine / pharmacology
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Oleic Acid / pharmacology
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Oleic Acids
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Pituitary Gland / drug effects
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Pituitary Gland / physiology*
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Pituitary Neoplasms
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Potassium Chloride / pharmacology*
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Prolactin / metabolism
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Rats
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Rats, Sprague-Dawley
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Stearic Acids / pharmacology
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Stereoisomerism
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Tumor Cells, Cultured
Substances
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Calcium Channels
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Fatty Acids, Nonesterified
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Fatty Acids, Unsaturated
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Oleic Acids
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Stearic Acids
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Gramicidin
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Oleic Acid
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Ethanol
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elaidic acid
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stearic acid
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Nimodipine
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Potassium Chloride
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Prolactin
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Growth Hormone
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Calcium