Abstract
The binding of omega-conotoxin to isolated rat neurohypophysial nerve terminals, its effect on the depolarization-induced increase of cytoplasmic Ca2+ and on the potassium and electrically-induced release of vasopressin (AVP) have been studied. The results show that isolated neurosecretory nerve endings have calcium channels with a high affinity for omega-CgTx and that this toxin inhibits neurohormone release at very low concentration (IC50 = 0. 1nM). Although secretion of vasopressin is inhibited to a great extent by the toxin it is shown that a small but significant amount of the depolarization-induced AVP release is insensitive to omega-CgTx and to the dihydropyridine molecule nicardipine.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Arginine Vasopressin / metabolism*
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Calcium Channel Blockers / pharmacology*
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Cell Membrane / physiology
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Dihydropyridines / pharmacology
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Electric Stimulation
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In Vitro Techniques
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Kinetics
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Male
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Mollusk Venoms / metabolism
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Mollusk Venoms / pharmacology*
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Nerve Endings / drug effects
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Nerve Endings / physiology*
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Nicardipine / pharmacology
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Pituitary Gland, Posterior / drug effects
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Pituitary Gland, Posterior / metabolism
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Pituitary Gland, Posterior / physiology*
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Potassium / pharmacology
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Rats
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Reference Values
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Verapamil / analogs & derivatives
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Verapamil / pharmacology
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omega-Conotoxin GVIA
Substances
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Calcium Channel Blockers
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Dihydropyridines
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Mollusk Venoms
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Arginine Vasopressin
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1,4-dihydropyridine
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omega-Conotoxin GVIA
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4-desmethoxyverapamil
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Verapamil
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Nicardipine
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Potassium