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Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine

Noninnervated cultured chick embryonic heart cells are depolarized by veratridine (10(-5) 10(-6) g/ml) within a few minutes to membrane potentials of -12 ± 2 mv. Action potentials and beating cease. Before depolarization begins, the repolarizing phase of the action potential is prolonged and leads t...

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Autores principales: Sperelakis, Nick, Pappano, Achilles J.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1969
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2202897/
https://www.ncbi.nlm.nih.gov/pubmed/5761875
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author Sperelakis, Nick
Pappano, Achilles J.
author_facet Sperelakis, Nick
Pappano, Achilles J.
author_sort Sperelakis, Nick
collection PubMed
description Noninnervated cultured chick embryonic heart cells are depolarized by veratridine (10(-5) 10(-6) g/ml) within a few minutes to membrane potentials of -12 ± 2 mv. Action potentials and beating cease. Before depolarization begins, the repolarizing phase of the action potential is prolonged and leads to a long-lasting depolarizing afterpotential, probably due to a holding open of Na(+) channels. There is no direct effect on automaticity. Maximum rate of rise of the action potential decreases as a function of the depolarization. The inexcitability is transiently reversed by repolarizing current pulses and by 5 mM Ba(++) (but not Sr(++)) which increases membrane resistance (R(m)) and produces a small transient repolarization. Cocaine does not reverse the depolarization. The depolarization also occurs in Cl(-)-free Ringer and in Na(+)-free Li(+)-Ringer, but not in Na(+)-free sucrose-Ringer. In most cases, R(m), measured in the presence and absence of Cl(-), initially decreases but sometimes increases. Some of the decrease or increase in g (K) may be indirectly produced by anomalous or delayed rectification, respectively. Tetrodotoxin, although having no effect on the action potential magnitude or rate of rise, prevents the depolarizing action of veratridine but not its effect on decreasing R(m). It is concluded that veratridine depolarizes by increasing the resting Na(+) permeability (P (Na)); it also tends to increase P (K), but this action may be obscured by anomalous rectification when E(m) is allowed to change. The equilibrium potential for veratridine action is about halfway between E (Na) and E (K), similar to that of acetylcholine at the vertebrate neuromuscular junction.
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spelling pubmed-22028972008-04-23 Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine Sperelakis, Nick Pappano, Achilles J. J Gen Physiol Article Noninnervated cultured chick embryonic heart cells are depolarized by veratridine (10(-5) 10(-6) g/ml) within a few minutes to membrane potentials of -12 ± 2 mv. Action potentials and beating cease. Before depolarization begins, the repolarizing phase of the action potential is prolonged and leads to a long-lasting depolarizing afterpotential, probably due to a holding open of Na(+) channels. There is no direct effect on automaticity. Maximum rate of rise of the action potential decreases as a function of the depolarization. The inexcitability is transiently reversed by repolarizing current pulses and by 5 mM Ba(++) (but not Sr(++)) which increases membrane resistance (R(m)) and produces a small transient repolarization. Cocaine does not reverse the depolarization. The depolarization also occurs in Cl(-)-free Ringer and in Na(+)-free Li(+)-Ringer, but not in Na(+)-free sucrose-Ringer. In most cases, R(m), measured in the presence and absence of Cl(-), initially decreases but sometimes increases. Some of the decrease or increase in g (K) may be indirectly produced by anomalous or delayed rectification, respectively. Tetrodotoxin, although having no effect on the action potential magnitude or rate of rise, prevents the depolarizing action of veratridine but not its effect on decreasing R(m). It is concluded that veratridine depolarizes by increasing the resting Na(+) permeability (P (Na)); it also tends to increase P (K), but this action may be obscured by anomalous rectification when E(m) is allowed to change. The equilibrium potential for veratridine action is about halfway between E (Na) and E (K), similar to that of acetylcholine at the vertebrate neuromuscular junction. The Rockefeller University Press 1969-01-01 /pmc/articles/PMC2202897/ /pubmed/5761875 Text en Copyright © 1969 by The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Sperelakis, Nick
Pappano, Achilles J.
Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine
title Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine
title_full Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine
title_fullStr Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine
title_full_unstemmed Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine
title_short Increase in P (Na) and P (K) of Cultured Heart Cells Produced by Veratridine
title_sort increase in p (na) and p (k) of cultured heart cells produced by veratridine
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2202897/
https://www.ncbi.nlm.nih.gov/pubmed/5761875
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