Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton

Autores
Venosa, Roque Alberto
Año de publicación
2003
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Hypotonicity produces a marked activation of the Na⁺ pump in frog sartorius muscle. The increase in net Na⁺ efflux under hypotonic conditions occurs despite the reductions in [Na⁺]i that are due to fibre swelling and Na⁺ loss. The pump density (ouabain binding) increases not only upon reduction of the medium osmotic pressure (π) from its normal value (π = 1) to one-half (π = 0.5), but also in muscles that are returned to π = 1 after equilibration in π = 2 medium. The equilibration in π = 2 medium does not affect pump density. Ouabain-binding increments cannot be ascribed to a rise in the Na⁺–K⁺ exchange rate of a fixed number of pumps: they also occurred in the continued presence of a saturating concentration of ouabain (50 μM). Under those conditions, the π = 1 → π = 0.5 transfer produced a 43 % increase in pump sites, while the π = 2 → π = 1 transfer induced a rise of 46 %. Actinomycin D did not alter the stimulation of Na⁺ extrusion elicited by hypotonicity, suggesting that de novo synthesis of pumps was not involved in the increase of the apparent number of pump sites. Disruption of microtubules by colchicine (100 μM) and intermediate filaments by acrylamide (4 mM) did not alter the hypotonic effect. Likewise, genistein (100 μM), a specific inhibitor of tyrosine kinase, did not affect significantly the hypotonic response. Microfilament-disrupting agents like cytochalasin B (5 μM) and latrunculin B (10 μM) reduced the increase in Na⁺ efflux induced by π = 1 → π = 0.5 transfer by about 35 % and 72 %, respectively. Latrunculin B reduced the increases in pump density generated by π = 1 → π = 0.5 and π = 2 → π = 1 transfers by about 79 % and 91 %, respectively. The results suggest that the membrane stretch due to hypotonic fibre volume increase would promote a microfilament-mediated insertion of submembranous spare Na⁺ pumps in the sarcolemma and, consequently, the rise in active Na⁺ transport.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
Materia
Medicina
hypotonicity
frog
sartorius muscle
Na⁺ active transport
cytoskeleton
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/127112

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network_name_str SEDICI (UNLP)
spelling Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeletonVenosa, Roque AlbertoMedicinahypotonicityfrogsartorius muscleNa⁺ active transportcytoskeletonHypotonicity produces a marked activation of the Na⁺ pump in frog sartorius muscle. The increase in net Na⁺ efflux under hypotonic conditions occurs despite the reductions in [Na⁺]<sub>i</sub> that are due to fibre swelling and Na⁺ loss. The pump density (ouabain binding) increases not only upon reduction of the medium osmotic pressure (π) from its normal value (π = 1) to one-half (π = 0.5), but also in muscles that are returned to π = 1 after equilibration in π = 2 medium. The equilibration in π = 2 medium does not affect pump density. Ouabain-binding increments cannot be ascribed to a rise in the Na⁺–K⁺ exchange rate of a fixed number of pumps: they also occurred in the continued presence of a saturating concentration of ouabain (50 μM). Under those conditions, the π = 1 → π = 0.5 transfer produced a 43 % increase in pump sites, while the π = 2 → π = 1 transfer induced a rise of 46 %. Actinomycin D did not alter the stimulation of Na⁺ extrusion elicited by hypotonicity, suggesting that <i>de novo</i> synthesis of pumps was not involved in the increase of the apparent number of pump sites. Disruption of microtubules by colchicine (100 μM) and intermediate filaments by acrylamide (4 mM) did not alter the hypotonic effect. Likewise, genistein (100 μM), a specific inhibitor of tyrosine kinase, did not affect significantly the hypotonic response. Microfilament-disrupting agents like cytochalasin B (5 μM) and latrunculin B (10 μM) reduced the increase in Na⁺ efflux induced by π = 1 → π = 0.5 transfer by about 35 % and 72 %, respectively. Latrunculin B reduced the increases in pump density generated by π = 1 → π = 0.5 and π = 2 → π = 1 transfers by about 79 % and 91 %, respectively. The results suggest that the membrane stretch due to hypotonic fibre volume increase would promote a microfilament-mediated insertion of submembranous spare Na⁺ pumps in the sarcolemma and, consequently, the rise in active Na⁺ transport.Facultad de Ciencias MédicasCentro de Investigaciones Cardiovasculares2003-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf451-459http://sedici.unlp.edu.ar/handle/10915/127112enginfo:eu-repo/semantics/altIdentifier/url/https://physoc.onlinelibrary.wiley.com/doi/10.1111/j.1469-7793.2003.00451.xinfo:eu-repo/semantics/altIdentifier/issn/0022-3751info:eu-repo/semantics/altIdentifier/issn/1469-7793info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:30:42Zoai:sedici.unlp.edu.ar:10915/127112Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:30:43.16SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
title Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
spellingShingle Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
Venosa, Roque Alberto
Medicina
hypotonicity
frog
sartorius muscle
Na⁺ active transport
cytoskeleton
title_short Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
title_full Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
title_fullStr Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
title_full_unstemmed Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
title_sort Hypotonic stimulation of the Na⁺ active transport in frog skeletal muscle: role of the cytoskeleton
dc.creator.none.fl_str_mv Venosa, Roque Alberto
author Venosa, Roque Alberto
author_facet Venosa, Roque Alberto
author_role author
dc.subject.none.fl_str_mv Medicina
hypotonicity
frog
sartorius muscle
Na⁺ active transport
cytoskeleton
topic Medicina
hypotonicity
frog
sartorius muscle
Na⁺ active transport
cytoskeleton
dc.description.none.fl_txt_mv Hypotonicity produces a marked activation of the Na⁺ pump in frog sartorius muscle. The increase in net Na⁺ efflux under hypotonic conditions occurs despite the reductions in [Na⁺]<sub>i</sub> that are due to fibre swelling and Na⁺ loss. The pump density (ouabain binding) increases not only upon reduction of the medium osmotic pressure (π) from its normal value (π = 1) to one-half (π = 0.5), but also in muscles that are returned to π = 1 after equilibration in π = 2 medium. The equilibration in π = 2 medium does not affect pump density. Ouabain-binding increments cannot be ascribed to a rise in the Na⁺–K⁺ exchange rate of a fixed number of pumps: they also occurred in the continued presence of a saturating concentration of ouabain (50 μM). Under those conditions, the π = 1 → π = 0.5 transfer produced a 43 % increase in pump sites, while the π = 2 → π = 1 transfer induced a rise of 46 %. Actinomycin D did not alter the stimulation of Na⁺ extrusion elicited by hypotonicity, suggesting that <i>de novo</i> synthesis of pumps was not involved in the increase of the apparent number of pump sites. Disruption of microtubules by colchicine (100 μM) and intermediate filaments by acrylamide (4 mM) did not alter the hypotonic effect. Likewise, genistein (100 μM), a specific inhibitor of tyrosine kinase, did not affect significantly the hypotonic response. Microfilament-disrupting agents like cytochalasin B (5 μM) and latrunculin B (10 μM) reduced the increase in Na⁺ efflux induced by π = 1 → π = 0.5 transfer by about 35 % and 72 %, respectively. Latrunculin B reduced the increases in pump density generated by π = 1 → π = 0.5 and π = 2 → π = 1 transfers by about 79 % and 91 %, respectively. The results suggest that the membrane stretch due to hypotonic fibre volume increase would promote a microfilament-mediated insertion of submembranous spare Na⁺ pumps in the sarcolemma and, consequently, the rise in active Na⁺ transport.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
description Hypotonicity produces a marked activation of the Na⁺ pump in frog sartorius muscle. The increase in net Na⁺ efflux under hypotonic conditions occurs despite the reductions in [Na⁺]<sub>i</sub> that are due to fibre swelling and Na⁺ loss. The pump density (ouabain binding) increases not only upon reduction of the medium osmotic pressure (π) from its normal value (π = 1) to one-half (π = 0.5), but also in muscles that are returned to π = 1 after equilibration in π = 2 medium. The equilibration in π = 2 medium does not affect pump density. Ouabain-binding increments cannot be ascribed to a rise in the Na⁺–K⁺ exchange rate of a fixed number of pumps: they also occurred in the continued presence of a saturating concentration of ouabain (50 μM). Under those conditions, the π = 1 → π = 0.5 transfer produced a 43 % increase in pump sites, while the π = 2 → π = 1 transfer induced a rise of 46 %. Actinomycin D did not alter the stimulation of Na⁺ extrusion elicited by hypotonicity, suggesting that <i>de novo</i> synthesis of pumps was not involved in the increase of the apparent number of pump sites. Disruption of microtubules by colchicine (100 μM) and intermediate filaments by acrylamide (4 mM) did not alter the hypotonic effect. Likewise, genistein (100 μM), a specific inhibitor of tyrosine kinase, did not affect significantly the hypotonic response. Microfilament-disrupting agents like cytochalasin B (5 μM) and latrunculin B (10 μM) reduced the increase in Na⁺ efflux induced by π = 1 → π = 0.5 transfer by about 35 % and 72 %, respectively. Latrunculin B reduced the increases in pump density generated by π = 1 → π = 0.5 and π = 2 → π = 1 transfers by about 79 % and 91 %, respectively. The results suggest that the membrane stretch due to hypotonic fibre volume increase would promote a microfilament-mediated insertion of submembranous spare Na⁺ pumps in the sarcolemma and, consequently, the rise in active Na⁺ transport.
publishDate 2003
dc.date.none.fl_str_mv 2003-04
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
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status_str publishedVersion
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info:eu-repo/semantics/altIdentifier/issn/0022-3751
info:eu-repo/semantics/altIdentifier/issn/1469-7793
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
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Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
dc.format.none.fl_str_mv application/pdf
451-459
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