Electrophysiology of posterior, Na-Cl absorbing gills Chasmagnathus granulatus: rapid responses to osmotic variations.

17. TRESGUERRES, M; ONKEN, H; PÉREZ, A; LUQUET, C.

JOURNAL OF EXPERIMENTAL BIOLOGY

The Company of Biologists

Lugar: Cambridge; Año: 2003 vol. 206 p. 619 - 626

0022-0949

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 l–1) was used instead of isosmotic solution (1045 mosmol l–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 mAcm–2 to –179.3±37.0 mAcm–2; Gte: from 40.5±16.9mScm–2 to 47.3±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 l–1) was used instead of isosmotic solution (1045 mosmol l–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 mAcm–2 to –179.3±37.0 mAcm–2; Gte: from 40.5±16.9mScm–2 to 47.3±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 l–1) was used instead of isosmotic solution (1045 mosmol l–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 mAcm–2 to –179.3±37.0 mAcm–2; Gte: from 40.5±16.9mScm–2 to 47.3±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 l–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 mAcm–2 to –179.3±37.0 mAcm–2; Gte: from 40.5±16.9mScm–2 to 47.3±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 mAcm–2 to –179.3±37.0 mAcm–2; Gte: from 40.5±16.9mScm–2 to 47.3±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg–1. 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 mAcm–2 to –179.3±37.0 mAcm–2; Gte: from 40.5±16.9mScm–2 to 47.3±15.8mScm–2). 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 h–1mg–1 to 41.84±14.54mmolPi h–1mg