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- Effect of blocking the Na+/K+ ATPase on Ca2+ extrusion and l...Effect of blocking the Na+/K+ ATPase on Ca2+ extrusion and light adaptation in mammalian retinal rods
Biophysical Journal, Volume 69, Issue 2, 1 August 1995, Pages 439-450
G.C. Demontis, G.M. Ratto, S. Bisti and L. Cervetto
AbstractMembrane current and light response were recorded from rods of monkey and guinea pig by means of suction electrodes. The correlation between adaptation and the Na+/K+ pump was investigated by measuring light-dependent changes in sensitivity with and without inhibition of Na+/K+ ATPase by strophanthidin. Strophanthidin was found to reduce the dark current, to slow the time course of the photoresponse, and to increase light sensitivity. At concentrations between 20 and 500 nM, the pump inhibitor suppressed in a reversible way the current re-activation occurring during prolonged illumination and modified the light-dependent decrease in sensitivity, which in control conditions approximates to a Weber-Fechner function. The effects of the pump inhibitor on the adaptive properties of rods are associated with an increased time constant of the membrane current attributed to the operation of the Na+:Ca2+,K+ exchanger. The effects of rapid application of the pump inhibitor on the current re-activation are consistent with the idea that significant changes in the internal sodium occur in rods of mammals during background illumination and that they play an important role in the process of light adaptation.
Abstract | PDF (1094 kb) - Na/K Pump Current and [Na]i in Rabbit Ventricular Myocytes: ...Na/K Pump Current and [Na]i in Rabbit Ventricular Myocytes: Local [Na]i Depletion and Na Buffering
Biophysical Journal, Volume 84, Issue 6, 1 June 2003, Pages 4157-4166
Sanda Despa and Donald M. Bers
AbstractNa/K pump current () and intracellular Na concentration ([Na]) were measured simultaneously in voltage-clamped rabbit ventricular myocytes, under conditions where [Na] is controlled mainly by membrane transport. Upon abrupt pump reactivation (after 10–12min blockade), decays in two phases. Initially, declines with little [Na] change, whereas the second phase is accompanied by [Na] decline. Initial sag was still present at external []=15mM, but prevented by [Na] ∼ 100mM. Initial sag might be explained by subsarcolemmal [Na] ([Na]) depletion produced by rapid Na extrusion and . Brief episodes of pump blockade allowed [Na] repletion, since peak postblockade exceeded at the end of previous activation (without appreciably altered global [Na]). The apparent for [Na] was higher for continuous activation than peak (14.1±0.2 vs. 11.2±0.2mM), whereas that based on [Na]/ matched peak (11.6±0.3mM). [Na] depletion (vs. [Na]) could be as high as 3mM for [Na] ∼ 18–20mM. A simple diffusion model indicates that such [Na] depletion requires a Na diffusion coefficient 10- to 10-fold below that expected in bulk cytoplasm (although this could be subsarcolemmal only). integrals and [Na] decline were used to estimate intracellular Na buffering, which is slight (1.39±0.09).
Abstract | Full Text | PDF (225 kb) - Action Potential and Contractility Changes in [Na]i Overload...Action Potential and Contractility Changes in [Na]i Overloaded Cardiac Myocytes: A Simulation Study
Biophysical Journal, Volume 78, Issue 5, 1 May 2000, Pages 2392-2404
Gregory M. Faber and Yoram Rudy
AbstractSodium overload of cardiac cells can accompany various pathologies and induce fatal cardiac arrhythmias. We investigate effects of elevated intracellular sodium on the cardiac action potential (AP) and on intracellular calcium using the Luo–Rudy model of a mammalian ventricular myocyte. The results are: 1) During rapid pacing, AP duration (APD) shortens in two phases, a rapid phase without Na accumulation and a slower phase that depends on [Na]. 2) The rapid APD shortening is due to incomplete deactivation (accumulation) of I. 3) The slow phase is due to increased repolarizing currents and reverse-mode , secondary to elevated [Na]. 4) Na-overload slows the rate of AP depolarization, allowing time for greater activation; it also enhances reverse-mode . The resulting increased Ca influx triggers a greater [Ca] transient. 5) Reverse-mode alone can trigger Ca release in a voltage and [Na]-dependent manner. 6) During block, Na and Ca accumulate and APD shortens due to enhanced reverse-mode ; contribution of to APD shortening is negligible. By slowing AP depolarization (hence velocity) and shortening APD, Na-overload acts to enhance inducibility of reentrant arrhythmias. Shortened APD with elevated [Ca] (secondary to Na-overload) also predisposes the myocardium to arrhythmogenic delayed afterdepolarizations.
Abstract | Full Text | PDF (264 kb) - …more
Copyright © 1982 The Biophysical Society. All rights reserved.
Biophysical Journal, Volume 40, Issue 3, 185-198, 1 December 1982
doi:10.1016/S0006-3495(82)84474-3
Research Article
Effect of strophanthidin on intracellular Na ion activity and twitch tension of constantly driven canine cardiac Purkinje fibers
C.O. Lee and M. Dagostino
Abstract
Intracellular Na ion activity (aiNa) and twitch tension (T) of constantly driven (1 Hz) canine cardiac Purkinje fibers were measured simultaneously and continuously with neutral carrier Na+-selective microelectrodes and a force transducer. The aiNa of 8.9 +/- 1.4 mM (mean +/- SD, n = 52) was obtained in the driven fibers perfused with normal Tyrode solution. Temporary interruption of stimulation showed that aiNa of the driven fibers was approximately 1.5 mM greater than that of quiescent fibers. The constantly driven fibers were exposed to strophanthidin of 10(-8), 5 X 10(-8), 10(-7), 5 X 10(-7), and 10(-6) M for 5min. No detectable changes in aiNa and T were observed in the fibers exposed to 10(-8) M strophanthidin, and the threshold concentration of the strophanthidin effect appeared to be approximately 5 X 10(-8) M. With concentrations greater than 5 X 10(-8) M, strophanthidin produced dose-dependent increases in aiNa and T. An increase in aiNa always accompanied an increase in T and after strophanthidin exposure both aiNa and T recovered completely. During onset and recovery periods of the strophanthidin effect the time course of change in aiNa was similar to that of change in T. A plot of T vs. aiNa during the onset and recovery periods showed a linear relationship between T and aiNa. These results indicate strongly that the positive inotropic effect of strophanthidin is closely associated with the increase in aiNa. Raising [K+]0 from 5.4 to 10.8 mM produced decreases in aiNa and T, and restoration of [K+]0 resulted in recoveries of aiNa and T. During the changes of [K+]0 the time course of change in aiNa was similar to that of the change in T. A steady-state sarcoplasmic Ca ion activity (aiCa) of 112 +/- 31 nM (mean +/- SD, n = 17) was obtained in the driven fibers with the use of neutral carrier Ca2+-selective microelectrodes. Temporary interruption produced 10–30% decreases in aiCa. No detectable changes in aiCa were observed in the fibers exposed to strophanthidin of 10(-7) M or less; 5 X 10(-7) and 10(-6) M strophanthidin produced 1.3–1.6 and 2–3-fold increases in aiCa, respectively. This result is consistent with the hypothesis that an increase in aiNa produces an increase in aiCa, which enhances Ca accumulation in the intracellular stores.
