Delayed Rectification in the Heart: Regulation and Physiology

Author(s):  
W. M. Kwok ◽  
L. C. Freeman ◽  
J. Anumonwo ◽  
R. S. Kass
1973 ◽  
Vol 61 (2) ◽  
pp. 176-184 ◽  
Author(s):  
Hiroshi Washio

The effect of glycerol treatment on the membrane currents and tension development was studied in voltage clamped snake muscle fibers. In muscle fibers which were exposed for 1 h to a normal saline containing 400 mM glycerol and then returned to a normal medium, graded depolarizations did not accompany contractile responses. However, when the fiber was depolarized to a certain level, an increment of outward current appeared which partially inactivated with time. The threshold for delayed rectification in glycerol-treated fibers was almost the same as that of intact fibers in spite of the absence of contractile tension. The results suggest that the delayed rectification may be attributed at least in part to the surface membrane and that the contractile activation probably does not depend simply on the inactivating outward currents through the delayed rectification channel.


1992 ◽  
Vol 262 (3) ◽  
pp. H921-H925 ◽  
Author(s):  
J. M. Anumonwo ◽  
L. C. Freeman ◽  
W. M. Kwok ◽  
R. S. Kass

We have studied delayed rectifier K+ currents (IK) in cells isolated from the sinoatrial node (SAN) region of the guinea pig. Using whole cell patch-clamp procedures, we measured the voltage dependence of IK activation and IK kinetics and the IK equilibrium potential in 4.8 mM extracellular K concentration solutions. Experiments were designed to contrast properties of guinea pig SAN IK with those of IK recorded from SAN cells of the rabbit. We find that guinea pig SAN IK differs from IK recorded from single rabbit SAN cells in its activation threshold, and in the absence of inactivation of whole cell currents recorded over a wide voltage range. These results, along with the relative insensitivity of guinea pig SAN IK to E-4031 and lanthanum, suggest that under our experimental conditions, a strongly rectifying IK component (IK,r) is not the major component of delayed rectification in the guinea pig SAN, as it appears to be in SAN cells of the rabbit.


Life Sciences ◽  
1968 ◽  
Vol 7 (7) ◽  
pp. 367-370 ◽  
Author(s):  
H. Lorkovic ◽  
C. Edwards

1976 ◽  
Vol 39 (2) ◽  
pp. 311-323 ◽  
Author(s):  
R. Llinas ◽  
C. Nicholson

1. The electrophysiological properties of the EPSP generated in Purkinje cells by the activation of CFs were studies in the cat cerebellar cortex. 2. CF-EPSPs were evoked by electrical stimulation of the cerebellar white matter and recorded intracellularly from the soma of the Purkinje cells. 3. Current was injected into the Purkinje cells via the recording micropipette using a bridge amplifer in order to study the reversal properties of the EPSP. 4. The CF-EPSP reversal was biphasic with the early portion reversing first. 5. The reversed EPSP waveform was not a mirror image of the EPSP, but displayed a briefer time course. 6. A four-compartment computer stimulation showed that the reversal properities of the CF-EPSP were explicable in terms of a distributed synapse on a cable. 7. The biphasic reversal and asymmetry were shown to be due to the spatially nonuniform potential distribution created by the somatic current injection, which predominantly reversed the proximal part of the distributed synapse. Delayed rectification may also have contributed to the reversal asymmetry. 8. The advantages of a distributed synapse over a point synapse are discussed and the reversal properties of the CF-EPSP compared to those of the Ia-evoked EPSP in motoneurons.


1966 ◽  
Vol 50 (2) ◽  
pp. 269-278 ◽  
Author(s):  
R. A. Sjodin

Giant axons from the squid were injected with 1.5 M cesium sulfate solutions containing the radioactive isotopes 42K and 134Cs. These axons, when stimulated, gave characteristic long duration action potentials lasting between 5 and 45 msec. The effluxes of 42K and 134Cs were measured both under resting conditions and during periods of repetitive stimulation. During the lengthened responses there were considerable increases in potassium efflux but only small increases in cesium efflux. The selectivity of the delayed rectification process was about 9 times greater for potassium ions than for cesium ions. The data suggest that internal cesium ions inhibit the outward potassium movement occurring during an action potential. The extra potassium effluxes taking place during excitation appear to be reduced in the presence of cesium ions to values between 7 and 22% of those expected in the absence of cesium inhibition.


1987 ◽  
Vol 128 (1) ◽  
pp. 1-17
Author(s):  
L. A. Orr ◽  
E. M. Lieberman

A lightly platinized tungsten (Pt-W) wire electrode, axially inserted into a crayfish giant axon, causes the development of cardiac-like action potentials with durations of up to 4 s. The plateau in membrane potential typically occurs within 10 min of the start of action potential elongation. The effect occurs without passing current through the Pt-W electrode and is temporally related to a dramatic decrease in intracellular pH (pHi). Such an effect cannot be induced by a decrease in pHi produced by equilibrating the axon with HCO3(−)-CO2 solution (pH6), and NH4Cl rebound or direct intracellular injection of PO4(3-) buffer (pH 4 X 5). Action potential elongation is accompanied by a block of delayed rectification and the possibility that inward rectification also develops cannot be ruled out. Plateau generation requires Na+ and Ca2+ inward currents as demonstrated by abolition of the plateau by [Na+]o or [Ca2+]o depletion or treatment with tetrodotoxin (TTX) or verapamil. The block of outward rectification by Pt-W requires external Na+ or Ca2+. Action potential elongation produced by 3,4-diaminopyridine is not sensitive to verapamil and the waveform is different from that produced by Pt-W. The data support the possibility that different classes of excitable membranes have similar channel populations and that the functional differences between them reside in the inhibitory or masking influences that are present in the microenvironments of the various membrane channels.


1962 ◽  
Vol 46 (1) ◽  
pp. 97-115 ◽  
Author(s):  
Shigehiro Nakajima ◽  
Shizuko Iwasaki ◽  
Kunihiko Obata

Delayed rectification was elicited in frog's skeletal muscles bathed in choline-Ringer's solution, in normal Ringer's solution with tetrodotoxin, in 40 mM Na2SO4 solution with tetrodotoxin, and even in 40 mM K2SO4 solution when the membrane had been previously hyperpolarized. However, after a sustained depolarization current-voltage relations in 40 mM K2SO4 and in 40 mM Na2SO4 solutions revealed a rectifier property in the anomalous direction. This indicates that the increase in potassium conductance which is brought about upon depolarization is a transient phenomenon and is inactivated by a maintained depolarization, and that this potassium inactivation process converts the delayed rectification into the anomalous rectification. In normal Ringer's solution with tetrodotoxin and in the 40 mM Na2SO4 solution with tetrodotoxin the apparent resistance was increased when the membrane was hyperpolarized beyond about -150 mv. This is thought to be due to a decrease of K conductance caused by a strong hyperpolarizing current. In the 40 mM Na2SO4 solution with tetrodotoxin a de- or hyperpolarizing current pulse induced a prolonged depolarizing response. During the early phase of this response the effective resistance was lower, and during the following phase greater than that in the resting fiber. An interpretation in terms of the ionic hypothesis was made of the nature of this response.


1960 ◽  
Vol 198 (5) ◽  
pp. 934-938 ◽  
Author(s):  
Toshio Narahashi ◽  
Takehiko Deguchi ◽  
Norimoto Urakawa ◽  
Yoshio Ohkubo

The mode of action of tetrodotoxin on the frog muscle fiber membrane has been analyzed with the aid of intracellular microelectrodes. Tetrodotoxin of 10–7 concentration made the applied cathodal current ineffective in producing action potential, whereas the resting potential and resting membrane resistance underwent little or no change. With 10–8 tetrodotoxin the muscle fibers responded with the small action potentials at high critical depolarizations. These results can be explained on the basis of the membrane being stabilized by inactivation of the sodium-carrying mechanism. Although delayed rectification was not observed in normal muscle fibers, it became apparent in the fibers rendered inexcitable by tetrodotoxin. This finding, together with other evidence in the existing literature, supports an applicability of the sodium theory to the frog muscle fibers.


1985 ◽  
Vol 48 (4) ◽  
pp. 553-567 ◽  
Author(s):  
P.B. Bennett ◽  
L.C. McKinney ◽  
R.S. Kass ◽  
T. Begenisich

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