Abstract
Adrenocorticotropic hormone (ACTH) is one of the principal activator of aldosterone secretion in rat zona glomerulosa cells, but its action on chloride currents is not well established. Here, we demonstrate that the hormone provoked a transient increase in a chloride current with a small unitary conductance estimated at 3.35 pS. Amplitude, as well as time-dependent increase of the ACTH-induced chloride current was independent of the intracellular cAMP concentration. In contrary, its decrease was sensitive to alkaline phosphatase and PKA-inhibitor H-89, indicating that protein phosphorylation, at least in part via PKA, is involved in the decline of the current.
MeSH terms
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1-Methyl-3-isobutylxanthine / pharmacology
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Adrenocorticotropic Hormone / pharmacology*
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Alkaline Phosphatase / metabolism
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Animals
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Cells, Cultured
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Chloride Channels / drug effects
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Chloride Channels / physiology
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Chlorides / metabolism*
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Cyclic AMP / metabolism
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Cyclic AMP-Dependent Protein Kinases / antagonists & inhibitors
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Electric Conductivity
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Female
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Isoquinolines / pharmacology
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Patch-Clamp Techniques
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Phosphorylation
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Rats
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Rats, Long-Evans
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Sulfonamides*
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Zona Glomerulosa / cytology
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Zona Glomerulosa / drug effects*
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Zona Glomerulosa / metabolism
Substances
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Chloride Channels
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Chlorides
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Isoquinolines
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Sulfonamides
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Adrenocorticotropic Hormone
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Cyclic AMP
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Cyclic AMP-Dependent Protein Kinases
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Alkaline Phosphatase
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N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide
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1-Methyl-3-isobutylxanthine