INVESTIGADORES
LUQUET Carlos Marcelo
artículos
Título:
Electrophysiology of posterior, Na-Cl absorbing gills Chasmagnathus granulatus: rapid responses to osmotic variations.
Autor/es:
17. TRESGUERRES, M; ONKEN, H; PÉREZ, A; LUQUET, C.
Revista:
JOURNAL OF EXPERIMENTAL BIOLOGY
Editorial:
The Company of Biologists
Referencias:
Lugar: Cambridge; Año: 2003 vol. 206 p. 619 - 626
ISSN:
0022-0949
Resumen:
In the present study, the influence of short-term
osmotic variations on some electrophysiological properties
related to NaCl absorption across posterior gills of
Chasmagnathus granulatus was investigated. The
transepithelial potential difference (Vte) of isolated and
perfused gills increased significantly when hyposmotic
saline (699 mosmol l1) was used instead of isosmotic
solution (1045 mosmol l1). A reduction of the
concentration of Na+ or Cl at constant osmolarity did not
produce any change in Vte. Transepithelial short-circuit
current (Isc) and conductance (Gte), measured with split
gill lamellae mounted in a modified Ussing chamber, also
increased after changing to hyposmotic salines (Isc: from
89.0±40.8 mAcm2 to 179.3±37.0 mAcm2; Gte: from
40.5±16.9mScm2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.was investigated. The
transepithelial potential difference (Vte) of isolated and
perfused gills increased significantly when hyposmotic
saline (699 mosmol l1) was used instead of isosmotic
solution (1045 mosmol l1). A reduction of the
concentration of Na+ or Cl at constant osmolarity did not
produce any change in Vte. Transepithelial short-circuit
current (Isc) and conductance (Gte), measured with split
gill lamellae mounted in a modified Ussing chamber, also
increased after changing to hyposmotic salines (Isc: from
89.0±40.8 mAcm2 to 179.3±37.0 mAcm2; Gte: from
40.5±16.9mScm2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte) of isolated and
perfused gills increased significantly when hyposmotic
saline (699 mosmol l1) was used instead of isosmotic
solution (1045 mosmol l1). A reduction of the
concentration of Na+ or Cl at constant osmolarity did not
produce any change in Vte. Transepithelial short-circuit
current (Isc) and conductance (Gte), measured with split
gill lamellae mounted in a modified Ussing chamber, also
increased after changing to hyposmotic salines (Isc: from
89.0±40.8 mAcm2 to 179.3±37.0 mAcm2; Gte: from
40.5±16.9mScm2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.1) was used instead of isosmotic
solution (1045 mosmol l1). A reduction of the
concentration of Na+ or Cl at constant osmolarity did not
produce any change in Vte. Transepithelial short-circuit
current (Isc) and conductance (Gte), measured with split
gill lamellae mounted in a modified Ussing chamber, also
increased after changing to hyposmotic salines (Isc: from
89.0±40.8 mAcm2 to 179.3±37.0 mAcm2; Gte: from
40.5±16.9mScm2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.1). A reduction of the
concentration of Na+ or Cl at constant osmolarity did not
produce any change in Vte. Transepithelial short-circuit
current (Isc) and conductance (Gte), measured with split
gill lamellae mounted in a modified Ussing chamber, also
increased after changing to hyposmotic salines (Isc: from
89.0±40.8 mAcm2 to 179.3±37.0 mAcm2; Gte: from
40.5±16.9mScm2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg1.
Theophylline maintained part of the elevated Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.Vte induced
by hyposmotic saline, suggesting that an increased cellular
cyclic AMP level is involved in the response to reduced
osmolarity. In summary, the results indicate that the
hemolymph osmolarity regulates active transbranchial
NaCl absorption by modulating the activity of the
basolateral Na+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+/K+-ATPase and by changing a conductive
pathway, probably at the apical membrane.+ or Cl at constant osmolarity did not
produce any change in Vte. Transepithelial short-circuit
current (Isc) and conductance (Gte), measured with split
gill lamellae mounted in a modified Ussing chamber, also
increased after changing to hyposmotic salines (Isc: from
89.0±40.8 mAcm2 to 179.3±37.0 mAcm2; Gte: from
40.5±16.9mScm2 to 47.3±15.8mScm2). The observed
effects of reduced osmolarity were fast, reversible and
gradually dependent on the magnitude of the osmotic
variation. The acitivity of the Na+/K+-ATPase increased
significantly after perfusion with hyposmotic saline, from
18.73±6.35mmolPi h1mg1 to 41.84±14.54mmolPi h1mg