Effect of calcium on the membrane potential of Amphiuma red cells.
An increase in extracellular Ca concentration causes the membrane of giant red cells of the salamander, Amphiuma means, to undergo a marked, transient hyperpolarization. This hyperpolarization is caused by an increase in K permeability of the membrane as judged from the K sensitivity of the membrane potential and from the rate of K loss under influence of raised extracellular Ca concentration. At constant external pH, the induction of hyperpolarization by increased extracellular Ca has a relatively well-defined threshold concentration. Furthermore the phenomenon is of an "all or none" type with most of the cells having membrane potential values either in the normal range (about -15 mV) or in the range -40 to -70mV. Shortly after suspension in Ringer's with 15 mm Ca, most if not all of the individual cells are hyperpolarized. Upon continued exposure (5-20 min) to the higher Ca concentration the membrane potential returns to the normal value in a fashion compatible with an "all or none" response. The observed Ca effect is sensitive to the pH of the suspending medium. At pH 6.2 the response is absent whereas the hyperpolarization is markedly stronger at pH 8.2 than at PH 7.2. It is argued that a reliable transport number for K under influence of Ca cannot be estimated from the slope of membrane potential vs. log (extracellular K concentration). This is probably related to the fact that the membrane potentials of the cells in the population do not stay constant in time. The above phenomenon is compared with the Ca-induced K permeability in poisoned human red cells or red cell ghosts. It is important to note that the cells employed in the present study are neither poisoned nor mechanically disrupted. This study emphasizes that the role of Ca in regulating cell membrane permeability to K seems to be a general feature.
Effect of calcium on the membrane potential of Amphiuma red cells. An increase in extracellular Ca concentration causes the membrane of giant red cells of the salamander, Amphiuma means, to undergo a marked, transient hyperpolarization. This hyperpolarization is caused by an increase in K permeability of the membrane as judged from the K sensitivity of the membrane potential and from the rate of K loss under influence of raised extracellular Ca concentration. At constant external pH, the induction of hyperpolarization by increased extracellular Ca has a relatively well-defined threshold concentration. Furthermore the phenomenon is of an "all or none" type with most of the cells having membrane potential values either in the normal range (about -15 mV) or in the range -40 to -70mV. Shortly after suspension in Ringer's with 15 mm Ca, most if not all of the individual cells are hyperpolarized. Upon continued exposure (5-20 min) to the higher Ca concentration the membrane potential returns to the normal value in a fashion compatible with an "all or none" response. The observed Ca effect is sensitive to the pH of the suspending medium. At pH 6.2 the response is absent whereas the hyperpolarization is markedly stronger at pH 8.2 than at PH 7.2. It is argued that a reliable transport number for K under influence of Ca cannot be estimated from the slope of membrane potential vs. log (extracellular K concentration). This is probably related to the fact that the membrane potentials of the cells in the population do not stay constant in time. The above phenomenon is compared with the Ca-induced K permeability in poisoned human red cells or red cell ghosts. It is important to note that the cells employed in the present study are neither poisoned nor mechanically disrupted. This study emphasizes that the role of Ca in regulating cell membrane permeability to K seems to be a general feature.