You searched for: electrogenic (Engelska - Spanska)

electrogenic sodium absorption
absorción electrógena de sodio

intestinal electrogenic chloride secretion
secreción intestinal electrógena de cloruro

electrogenic sodium absorption, function
absorción electrógena de sodio

intestinal electrogenic chloride secretion, function
secreción intestinal electrógena de cloruro

electrogenic sodium absorption, function (observable entity)
absorción electrógena de sodio

the process is electrogenic, the stoichiometry being <PROTECTED>+:2k+.
el proceso es electrógeno, con una estequiometría de <PROTECTED>+:2k+.

intestinal electrogenic chloride secretion, function (observable entity)
secreción intestinal electrógena de cloruro

because of its electrogenic properties, the atlantic torpedo was used in medicine by the ancient greeks and romans and became the namesake of the naval weapon.
debido a sus propiedades electrogénicas, los antiguos griegos y romanos utilizaban al torpedo del atlántico en la medicina e inspiró el nombre del arma naval homónima.

hellothe na -ca2 exchanger (ncx) links transmembrane movements of ca2 ions to the reciprocal movement of na ions. it normally functions primarily as a ca2 efflux mechanism in excitable tissues such as the heart, but it can also mediate ca2 influx under certain conditions. na and ca2 ions exert complex regulatory effects on ncx activity. ca2 binds to two regulatory sites in the exchanger’s central hydrophilic domain, and this interaction is normally essential for activation of exchange activity. high cytosolic na concentrations, however, can induce a constitutive activity that bypasses the need for allosteric ca2 activation. constitutive ncx activity can also be induced by high levels of phosphatidylinositol- 4,5-bisphosphate (pip2) and by mutations affecting the regulatory calcium binding domains. in addition to promoting constitutive activity, high cytosolic na concentrations also induce an inactivated state of the exchanger (na -dependent inactivation) that becomes dominant when cytosolic ph and pip2 levels fall. na -dependent inactivation may provide a means of protecting cells from ca2 overload due to ncx-mediated ca2 influx during ischemia. na /ca2 exchange (ncx) is a carrier-mediated transport process that translocates ca2 ions across membranes in an obligatory exchange for na ions. in excitable tissues such as heart and nerve, it functions primarily as a plasma membrane ca2 efflux mechanism, although it can also mediate ca2 influx given the appropriate thermodynamic gradients. ncx activity is regulated principally by the ions that comprise the major determinants of the ncx driving forces, i.e., cytosolic na and ca2 . increases in cytosolic na downregulate ncx activity by inducing an inactive state of the exchanger (na -dependent inactivation), whereas increases in cytosolic ca2 upregulate activity (through allosteric ca2 activation). here we will briefly review the history and molecular biology of na /ca2 exchange, describe the major characteristics of na -dependent inactivation and allosteric ca2 activation, and discuss issues related to the possible physiological roles of these regulatory mechanisms. we will focus mainly on the cardiac isoform of the na /ca2 exchanger (ncx1.1). the na /ca2 exchange family of transporters has been the subject of several recent reviews.1-3 a brief history of na /ca2 exchange the existence of a transporter linking oppositely-directed movements of na and ca2 across the plasma membrane was first described 40 years ago by two groups working (independently and respectively) with squid giant axons4 and guinea pig atria.5 it was immediately recognized that this novel transporter could be crucial to the understanding of the inotropic effects of cardiac glycosides. experimental work in the two decades that followed, done mostly with internally dialyzed squid axons or barnacle muscle, did much to establish the basic features of na /ca2 exchange and its regulation by atp and by cytosolic ca2 (see review by blaustein and lederer6). in 1979, the introduction of plasma membrane vesicles for exchange studies provided an important biochemical tool for further characterization of exchange activity. the stoichiometry of the exchanger was demonstrated to be 3na /1ca2 in null-point studies with vesicles where the electrical potential as a driving force for exchange activity was offset by an oppositely directed na -gradient.7 this value is still generally accepted although there have recently been indications from exchange current measurements of higher stoichiometries.8,9 the situation is complicated by the existence of a na -ca2 co-transport mode of the exchanger which provides an electrogenic na -leak current when na plus ca2 exchanges for ca2 alone.10 the use of plasma membrane vesicles also provided a route for the purification and identification of the exchanger protein using detergent solubilization, protein purification and vesicle reconstitution techniques. philipson and his colleagues11 succeeded in cloning the cardiac exchanger (ncx1) in 1990. the philipson group later described additional genes coding for ncx2 and ncx3 (both expressed primarily in brain and skeletal muscle). the cdna for the na /ca2 exchanger in squid axons, in which so much early work was carried out, was cloned in 1998;12 the squid axon exchanger (ncx-sq1) showed 58% identity to mammalian ncx1. electrical currents due to na /ca2 exchange activity were first demonstrated definitively by kimura et al.13 electrophysiological studies of na /ca2 exchange were markedly enhanced by the use of giant membrane patches, initially from cardiac myocytes and later from xenopus oocytes expressing the exchanger.14,15 the giant patch technology allowed the fluid composition on both sides of the membrane to be controlled and provided access to the cytosolic membrane surface for biochemical modification.
holathe na -ca2 exchanger (ncx) links transmembrane movements of ca2 ions to the reciprocal movement of na ions. it normally functions primarily as a ca2 efflux mechanism in excitable tissues such as the heart, but it can also mediate ca2 influx under certain conditions. na and ca2 ions exert complex regulatory effects on ncx activity. ca2 binds to two regulatory sites in the exchanger’s central hydrophilic domain, and this interaction is normally essential for activation of exchange activity. high cytosolic na concentrations, however, can induce a constitutive activity that bypasses the need for allosteric ca2 activation. constitutive ncx activity can also be induced by high levels of phosphatidylinositol- 4,5-bisphosphate (pip2) and by mutations affecting the regulatory calcium binding domains. in addition to promoting constitutive activity, high cytosolic na concentrations also induce an inactivated state of the exchanger (na -dependent inactivation) that becomes dominant when cytosolic ph and pip2 levels fall. na -dependent inactivation may provide a means of protecting cells from ca2 overload due to ncx-mediated ca2 influx during ischemia. na /ca2 exchange (ncx) is a carrier-mediated transport process that translocates ca2 ions across membranes in an obligatory exchange for na ions. in excitable tissues such as heart and nerve, it functions primarily as a plasma membrane ca2 efflux mechanism, although it can also mediate ca2 influx given the appropriate thermodynamic gradients. ncx activity is regulated principally by the ions that comprise the major determinants of the ncx driving forces, i.e., cytosolic na and ca2 . increases in cytosolic na downregulate ncx activity by inducing an inactive state of the exchanger (na -dependent inactivation), whereas increases in cytosolic ca2 upregulate activity (through allosteric ca2 activation). here we will briefly review the history and molecular biology of na /ca2 exchange, describe the major characteristics of na -dependent inactivation and allosteric ca2 activation, and discuss issues related to the possible physiological roles of these regulatory mechanisms. we will focus mainly on the cardiac isoform of the na /ca2 exchanger (ncx1.1). the na /ca2 exchange family of transporters has been the subject of several recent reviews.1-3 a brief history of na /ca2 exchange the existence of a transporter linking oppositely-directed movements of na and ca2 across the plasma membrane was first described 40 years ago by two groups working (independently and respectively) with squid giant axons4 and guinea pig atria.5 it was immediately recognized that this novel transporter could be crucial to the understanding of the inotropic effects of cardiac glycosides. experimental work in the two decades that followed, done mostly with internally dialyzed squid axons or barnacle muscle, did much to establish the basic features of na /ca2 exchange and its regulation by atp and by cytosolic ca2 (see review by blaustein and lederer6). in 1979, the introduction of plasma membrane vesicles for exchange studies provided an important biochemical tool for further characterization of exchange activity. the stoichiometry of the exchanger was demonstrated to be 3na /1ca2 in null-point studies with vesicles where the electrical potential as a driving force for exchange activity was offset by an oppositely directed na -gradient.7 this value is still generally accepted although there have recently been indications from exchange current measurements of higher stoichiometries.8,9 the situation is complicated by the existence of a na -ca2 co-transport mode of the exchanger which provides an electrogenic na -leak current when na plus ca2 exchanges for ca2 alone.10 the use of plasma membrane vesicles also provided a route for the purification and identification of the exchanger protein using detergent solubilization, protein purification and vesicle reconstitution techniques. philipson and his colleagues11 succeeded in cloning the cardiac exchanger (ncx1) in 1990. the philipson group later described additional genes coding for ncx2 and ncx3 (both expressed primarily in brain and skeletal muscle). the cdna for the na /ca2 exchanger in squid axons, in which so much early work was carried out, was cloned in 1998;12 the squid axon exchanger (ncx-sq1) showed 58% identity to mammalian ncx1. electrical currents due to na /ca2 exchange activity were first demonstrated definitively by kimura et al.13 electrophysiological studies of na /ca2 exchange were markedly enhanced by the use of giant membrane patches, initially from cardiac myocytes and later from xenopus oocytes expressing the exchanger.14,15 the giant patch technology allowed the fluid composition on both sides of the membrane to be controlled and provided access to the cytosolic membrane surface for biochemical modification.