Effect of caffeine on K+ efflux in frog skeletal muscle

Autores
Venosa, Roque Alberto; Hoya, Arturo
Año de publicación
1999
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The exposure of frog skeletal muscle to caffeine (3–4 mM) generates an increase of the K+ (42K+) efflux rate coefficient (k; K,o) which exhibits the following characteristics. First it is promoted by the rise in cytosolic Ca2+ ([Ca2+]i), because the effect is mimicked by ionomycin (1.25 µM), a Ca2+ ionophore. Second, the inhibition of caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) by 40 µM tetracaine significantly reduced the increase in k; K,o (Δk; K,o). Third, charybdotoxin (23 nM), a blocker of the large-conductance Ca2+-dependent K+ channels (BKCa channels) reduced Δk; K,o by 22%. Fourth, apamin (10 nM), a blocker of the small-conductance Ca2+-dependent K+ channels (SKCa channels), did not affect Δk; K,o. Fifth, tolbutamide (800 µM), an inhibitor of KATP channels, reduced Δk; K,o by about 23%. Sixth, Ba2+, a blocker of most K+ channels, did not preclude the caffeine-induced Δk; K,o. Seventh, omitting Na+ from the external medium reduced Δk; K,o by about 40%. Eight, amiloride (5 mM) decreased Δk; K,o by 65%. It is concluded that the caffeine-induced rise of [Ca2+]i increases K+ efflux, through the activation of: (1) two channels (BKCa and KATP) and (2) an external Na+-dependent amiloride-sensitive process.
Centro de Investigaciones Cardiovasculares
Materia
Ciencias Médicas
Caffeine
Calcium
Efflux
Frog
Potassium
Skeletal muscle
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/145104

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network_name_str SEDICI (UNLP)
spelling Effect of caffeine on K+ efflux in frog skeletal muscleVenosa, Roque AlbertoHoya, ArturoCiencias MédicasCaffeineCalciumEffluxFrogPotassiumSkeletal muscleThe exposure of frog skeletal muscle to caffeine (3–4 mM) generates an increase of the K+ (42K+) efflux rate coefficient (k; K,o) which exhibits the following characteristics. First it is promoted by the rise in cytosolic Ca2+ ([Ca2+]i), because the effect is mimicked by ionomycin (1.25 µM), a Ca2+ ionophore. Second, the inhibition of caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) by 40 µM tetracaine significantly reduced the increase in k; K,o (Δk; K,o). Third, charybdotoxin (23 nM), a blocker of the large-conductance Ca2+-dependent K+ channels (BKCa channels) reduced Δk; K,o by 22%. Fourth, apamin (10 nM), a blocker of the small-conductance Ca2+-dependent K+ channels (SKCa channels), did not affect Δk; K,o. Fifth, tolbutamide (800 µM), an inhibitor of KATP channels, reduced Δk; K,o by about 23%. Sixth, Ba2+, a blocker of most K+ channels, did not preclude the caffeine-induced Δk; K,o. Seventh, omitting Na+ from the external medium reduced Δk; K,o by about 40%. Eight, amiloride (5 mM) decreased Δk; K,o by 65%. It is concluded that the caffeine-induced rise of [Ca2+]i increases K+ efflux, through the activation of: (1) two channels (BKCa and KATP) and (2) an external Na+-dependent amiloride-sensitive process.Centro de Investigaciones Cardiovasculares1999-01-18info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf417-422http://sedici.unlp.edu.ar/handle/10915/145104enginfo:eu-repo/semantics/altIdentifier/issn/0031-6768info:eu-repo/semantics/altIdentifier/issn/1432-2013info:eu-repo/semantics/altIdentifier/doi/10.1007/s004240050796info:eu-repo/semantics/altIdentifier/pmid/9914398info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:32:12Zoai:sedici.unlp.edu.ar:10915/145104Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:32:13.256SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Effect of caffeine on K+ efflux in frog skeletal muscle
title Effect of caffeine on K+ efflux in frog skeletal muscle
spellingShingle Effect of caffeine on K+ efflux in frog skeletal muscle
Venosa, Roque Alberto
Ciencias Médicas
Caffeine
Calcium
Efflux
Frog
Potassium
Skeletal muscle
title_short Effect of caffeine on K+ efflux in frog skeletal muscle
title_full Effect of caffeine on K+ efflux in frog skeletal muscle
title_fullStr Effect of caffeine on K+ efflux in frog skeletal muscle
title_full_unstemmed Effect of caffeine on K+ efflux in frog skeletal muscle
title_sort Effect of caffeine on K+ efflux in frog skeletal muscle
dc.creator.none.fl_str_mv Venosa, Roque Alberto
Hoya, Arturo
author Venosa, Roque Alberto
author_facet Venosa, Roque Alberto
Hoya, Arturo
author_role author
author2 Hoya, Arturo
author2_role author
dc.subject.none.fl_str_mv Ciencias Médicas
Caffeine
Calcium
Efflux
Frog
Potassium
Skeletal muscle
topic Ciencias Médicas
Caffeine
Calcium
Efflux
Frog
Potassium
Skeletal muscle
dc.description.none.fl_txt_mv The exposure of frog skeletal muscle to caffeine (3–4 mM) generates an increase of the K+ (42K+) efflux rate coefficient (k; K,o) which exhibits the following characteristics. First it is promoted by the rise in cytosolic Ca2+ ([Ca2+]i), because the effect is mimicked by ionomycin (1.25 µM), a Ca2+ ionophore. Second, the inhibition of caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) by 40 µM tetracaine significantly reduced the increase in k; K,o (Δk; K,o). Third, charybdotoxin (23 nM), a blocker of the large-conductance Ca2+-dependent K+ channels (BKCa channels) reduced Δk; K,o by 22%. Fourth, apamin (10 nM), a blocker of the small-conductance Ca2+-dependent K+ channels (SKCa channels), did not affect Δk; K,o. Fifth, tolbutamide (800 µM), an inhibitor of KATP channels, reduced Δk; K,o by about 23%. Sixth, Ba2+, a blocker of most K+ channels, did not preclude the caffeine-induced Δk; K,o. Seventh, omitting Na+ from the external medium reduced Δk; K,o by about 40%. Eight, amiloride (5 mM) decreased Δk; K,o by 65%. It is concluded that the caffeine-induced rise of [Ca2+]i increases K+ efflux, through the activation of: (1) two channels (BKCa and KATP) and (2) an external Na+-dependent amiloride-sensitive process.
Centro de Investigaciones Cardiovasculares
description The exposure of frog skeletal muscle to caffeine (3–4 mM) generates an increase of the K+ (42K+) efflux rate coefficient (k; K,o) which exhibits the following characteristics. First it is promoted by the rise in cytosolic Ca2+ ([Ca2+]i), because the effect is mimicked by ionomycin (1.25 µM), a Ca2+ ionophore. Second, the inhibition of caffeine-induced Ca2+ release from the sarcoplasmic reticulum (SR) by 40 µM tetracaine significantly reduced the increase in k; K,o (Δk; K,o). Third, charybdotoxin (23 nM), a blocker of the large-conductance Ca2+-dependent K+ channels (BKCa channels) reduced Δk; K,o by 22%. Fourth, apamin (10 nM), a blocker of the small-conductance Ca2+-dependent K+ channels (SKCa channels), did not affect Δk; K,o. Fifth, tolbutamide (800 µM), an inhibitor of KATP channels, reduced Δk; K,o by about 23%. Sixth, Ba2+, a blocker of most K+ channels, did not preclude the caffeine-induced Δk; K,o. Seventh, omitting Na+ from the external medium reduced Δk; K,o by about 40%. Eight, amiloride (5 mM) decreased Δk; K,o by 65%. It is concluded that the caffeine-induced rise of [Ca2+]i increases K+ efflux, through the activation of: (1) two channels (BKCa and KATP) and (2) an external Na+-dependent amiloride-sensitive process.
publishDate 1999
dc.date.none.fl_str_mv 1999-01-18
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
Articulo
http://purl.org/coar/resource_type/c_6501
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format article
status_str publishedVersion
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dc.language.none.fl_str_mv eng
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info:eu-repo/semantics/altIdentifier/issn/1432-2013
info:eu-repo/semantics/altIdentifier/doi/10.1007/s004240050796
info:eu-repo/semantics/altIdentifier/pmid/9914398
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
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rights_invalid_str_mv http://creativecommons.org/licenses/by/4.0/
Creative Commons Attribution 4.0 International (CC BY 4.0)
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instname:Universidad Nacional de La Plata
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