Effect of high K, low K, and quinidine on QRS duration and ventricular action potential

1962 ◽  
Vol 203 (6) ◽  
pp. 1135-1140 ◽  
Author(s):  
Leonard S. Gettes ◽  
Borys Surawicz ◽  
James C. Shiue
Keyword(s):  
Action Potential ◽  
Resting Potential ◽  
Qrs Complex ◽  
High Potassium ◽  
Conduction Disturbances ◽  
High K ◽  
Low Potassium ◽  
Qrs Duration ◽  
Low K ◽  
Upstroke Velocity

Perfusion of isolated rabbit hearts with high potassium, low potassium, and quinidine solutions caused a diffuse widening of the QRS complex with no change in shape. These QRS changes were correlated with the magnitude and upstroke velocity of the ventricular transmembrane potential. An increase of QRS duration by 132% produced by high K was accompanied by a decrease of the action potential, resting potential, and upstroke velocity. A similar increase in QRS duration produced by quinidine was accompanied by a slow upstroke velocity but no change in magnitude of the action potential or resting potential. An increase of QRS duration by 49% produced by low K was accompanied by an increased action and resting potential, and upstroke velocity. We attributed the QRS changes produced by high K and quinidine, at least partly, to a slow conduction in the ventricle, caused by a slow upstroke velocity of the action potential. The QRS changes produced by low K could be explained by hyperpolarization. Early arrhythmias caused by low K were due to atrioventricular conduction disturbances.

scholarly journals Protonation state of E71 in KcsA and its role for channel collapse and inactivation

2012 ◽  
Vol 109 (38) ◽  
pp. 15265-15270 ◽  
Author(s):  
Manasi P. Bhate ◽  
Ann E. McDermott
Keyword(s):  
Resistant Mutant ◽  
Structural Rearrangement ◽  
Nmr Studies ◽  
High Potassium ◽  
Chemical Shift Tensors ◽  
Channel Inactivation ◽  
Potassium Channel Kcsa ◽  
High K ◽  
Low Potassium ◽  
Low K

The prototypical prokaryotic potassium channel KcsA alters its pore depending on the ambient potassium; at high potassium, it exists in a conductive form, and at low potassium, it collapses into a nonconductive structure with reduced ion occupancy. We present solid-state NMR studies of KcsA in which we test the hypothesis that an important channel-inactivation process, known as C-type inactivation, proceeds via a state similar to this collapsed state. We test this using an inactivation-resistant mutant E71A, and show that E71A is unable to collapse its pore at both low potassium and low pH, suggesting that the collapsed state is structurally similar to the inactivated state. We also show that E71A has a disordered selectivity filter. Using site-specific K+ titrations, we detect a local change at E71 that is coupled to channel collapse at low K+. To gain more insight into this change, we site specifically measure the chemical shift tensors of the side-chain carboxyls of E71 and its hydrogen bond partner D80, and use the tensors to assign protonation states to E71 and D80 at high K+ and neutral pH. Our measurements show that E71 is protonated at pH 7.5 and must have an unusually perturbed pKa (> 7.5) suggesting that the change at E71 is a structural rearrangement rather than a protonation event. The results offer new mechanistic insights into why the widely used mutant KcsA–E71A does not inactivate and establish the ambient K+ level as a means to populate the inactivated state of KcsA in a controlled way.

Effect of Several Cations on Transmembrane Potentials of Cardiac Muscle

1956 ◽  
Vol 186 (2) ◽  
pp. 317-324 ◽  
Author(s):  
Brian F. Hoffman ◽  
E. E. Suckling
Keyword(s):  
Action Potential ◽  
Cardiac Muscle ◽  
Action Potentials ◽  
Time Course ◽  
Pacemaker Activity ◽  
Transmembrane Potentials ◽  
High K ◽  
Intracellular Microelectrodes ◽  
Simultaneous Decrease ◽  
Low K

The effects of changes in the extracellular concentrations of Ca, K and Mg on the transmembrane resting and action potentials of single fibers of the auricle, ventricle and specialized conducting system of the dog heart have been studied by means of intracellular microelectrodes. With respect to Ca, the three tissues exhibit quite different sensitivities. Changes in concentration of this ion alter the time course of the action potential recorded from auricle and ventricle but have little effect on the action potential configuration of the Purkinje fiber. In the latter tissue, on the other hand, pacemaker activity is most strongly enhanced by Ca depletion and excitability is lost at Ca concentrations permitting normal propagation in papillary muscle. The effect of K on the resting transmembrane potential is dependent on the simultaneous Ca concentration. The interrelationship is such that the depolarizing effect of high K is decreased by elevated Ca and the depolarization produced by low K is diminished by low levels of Ca. Changes in the concentration of Mg have little effect on the transmembrane potentials of cardiac muscle unless the level of Ca is low. Under this condition a simultaneous decrease in Mg gives rise to a marked prolongation of the action potential duration of both auricle and ventricle. Some evidence for the basic similarity of the processes underlying repolarization in these three tissues is presented and it is thought the normally encountered differences in their action potentials may be related to the sensitivity of each tissue to extracellular Ca.

High Intake of Magnesium in Relation to the Ruminal Transmural Potential Difference and Magnesium Absorption in Wethers

2004 ◽  
Vol 74 (3) ◽  
pp. 217-222
Author(s):  
Jittakhot ◽  
Schonewille ◽  
Haddad ◽  
Wouterse ◽  
Yuangklang ◽  
...  
Keyword(s):  
Dry Matter ◽  
Latin Square ◽  
Potential Difference ◽  
High Intake ◽  
Individual Values ◽  
High Potassium ◽  
High K ◽  
The Mean ◽  
The Individual ◽  
Low K

High potassium (K) intakes are known to decrease magnesium (Mg) absorption in ruminants by increasing the transmural potential difference (PDt, serosal side = positive). High Mg intakes are known to increase the amount of Mg absorbed, which may be explained by increasing the ruminal Mg concentration, but an effect on the PDt cannot be excluded. The objective of this study was to determine whether or not Mg intake affects the PDt. In a 3x3 Latin square design, six ruminally fistulated wethers were fed a low-Mg, low-K ration (3.88 g Mg/kg dry matter (DM); 30.7 g K/kg DM), a high-Mg, low K-ration (16.79 g Mg/kg DM; 30.7 g K/kg DM), and a low-Mg ration high-K (3.88 g Mg/kg DM or 62.1 g K/kg DM). When compared with the low-Mg, low-K ration, the high-Mg, low-K ration raised the absolute apparent Mg absorption (g/day) by 421% and the low-Mg, high-K ration decreased it by 20%. The intake of extra K produced a significant increase in the PDt. The intake of extra Mg did not change the PDt across the rumen wall but produced a significant increase of the ruminal Mg concentrations. On the basis of the individual values for three rations, the mean post feeding ruminal Mg concentrations were found to be unrelated to the PDt (Pearson's r = –0.329, p = 0.183, n = 18). Thus, it is concluded that the observed increase in Mg absorption after a high Mg intake can be explained by an increase in the ruminal Mg concentration rather than by a change in PDt.

Mechanisms underlying the modulation of arrhythmogenic events by components of ischemia in guinea pig cardiac myocytes

1994 ◽  
Vol 72 (4) ◽  
pp. 382-393 ◽  
Author(s):  
Qi-Ying Liu ◽  
Mario Vassalle
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Voltage Clamp ◽  
Action Potentials ◽  
Ventricular Myocytes ◽  
Resting Potential ◽  
Spontaneous Discharge ◽  
High K ◽  
Voltage Dependent ◽  
Dependent Mechanism

The effects of some components of ischemia on the oscillatory (Vos) and nonoscillatory (Vex) potentials and respective currents (Ios and Iex), as well as their mechanisms, were studied in guinea pig isolated ventricular myocytes by means of a single-microelectrode, discontinuous voltage clamp method. Repetitive activations induced not only Vos and Ios, but also Vex and Iex. A small decrease in resting potential caused an immediate increase in Vos followed by a gradual increase due to the longer action potential. Immediate and gradual increases in Ios also occurred during voltage clamp steps. A small depolarization increased Vos and Vex, and facilitated the induction of spontaneous discharge by fast drive. At Vh where INa is inactivated, depolarizing steps induced larger Ios and Iex, indicating the importance of the Na-independent Ca loading. High [K]odecreased the resting potential, but also Vos, Vex, Ios, Iex, and ICa. In high [K]o, depolarization still increased Vos and Vex. Norepinephrine (NE) enhanced Vos and Vex, and also Ios and Iex, during voltage clamp steps. High [K]o antagonized NE effects, and NE those of high [K]o. In conclusion, on depolarization, Vos and Ios immediately increase through a voltage-dependent mechanism; and then Vos and Ios gradually increase, apparently through an increased Ca load related to the longer action potentials and the Na–Ca exchange. The depolarization induced by Vex may contribute to increase Vos size. Vos and Vex are similarly influenced by different procedures that modify Ca load. The arrhythmogenic events are enhanced by the simultaneous presence of depolarization, faster rate, or NE. Instead, high [K]o decreases Vos and Vex by decreasing ICa and opposes the effects of NE. The voltage clamp results show that potentiation and antagonism between different components of ischemia are due primarily to changes in Ca loading and not to changes in action potential configuration.Key words: ischemia, arrhythmias, oscillatory and nonoscillatory potentials and currents, norepinephrine, potassium.

scholarly journals Active Cation Transport and Ouabain Binding in High Potassium and Low Potassium Red Blood Cells of Sheep

1971 ◽  
Vol 58 (1) ◽  
pp. 94-116 ◽  
Author(s):  
Philip B. Dunham ◽  
Joseph F. Hoffman
Keyword(s):  
Binding Sites ◽  
High Specificity ◽  
Cation Transport ◽  
Nonspecific Binding ◽  
Ouabain Binding ◽  
High Potassium ◽  
High K ◽  
Low Potassium ◽  
The Difference ◽  
Specificity Of Binding

Red cells from high K sheep contained 82 mM K/liter cells and had a pump flux of 0.86 mM K/liter cells x hr; similarly, LK cells had 16.5 mM K/liter cells and a pump flux of 0.12 mM K/liter cells x hr. Using [3H]-ouabain, the relation between the number of ouabain molecules bound per cell and the concomitant per cent inhibition of the pump was found to be approximately linear for both HK and LK cells. The number of glycoside molecules necessary for 100 % inhibition of the pump was 42 for HK cells and 7.6 for LK cells, after correction for six nonspecific binding sites for each type of cell. The ratio of ouabain molecules/cell at 100 % inhibition was 5.5, HK to LK, and the ratio of the normal K pump fluxes was 7.2, HK to LK. The similarity of these ratios suggests that an important difference between HK and LK cells, determining the difference in pump fluxes, is the number of pump sites. The turnover times (ions/site x min) are 6000 and 4800 for HK and LK cells, respectively. The results also indicate a high specificity of binding of ouabain to pump sites.

scholarly journals Effects of high extracellular [K+] and adrenaline on force development, relaxation and membrane potential in cardiac muscle from freshwater turtle and rainbow trout

2001 ◽  
Vol 204 (2) ◽  
pp. 261-268 ◽  
Author(s):  
J.S. Nielsen ◽  
H. Gesser
Keyword(s):  
Rainbow Trout ◽  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Freshwater Turtle ◽  
Force Amplitude ◽  
Excitation Contraction Coupling ◽  
Twitch Force ◽  
Contraction Coupling ◽  
High K ◽  
Low K

Increases in extracellular K(+) concentrations reduced the twitch force amplitude of heart muscle from the freshwater turtle (Trachemys scripta elegans) and rainbow trout (Oncorhynchus mykiss). Adrenaline augmented twitch force amplitude and reduced the relative influence of [K(+)]. In the absence of adrenaline, high [K(+)] had less effect in reducing twitch force in turtle than in trout, whereas the reverse was true in the presence of adrenaline. Under anoxic conditions, twitch force was lower in 10 mmol l(−1) than in 2.5 mmol l(−1) K(+) in both preparations, but adrenaline removed this difference. A further analysis of turtle myocardium showed that action potential duration was shorter and resting potential more positive in high [K(+)] than in low [K(+)]. Adrenaline restored the duration of the action potential, but did not affect the depolarisation, which may attenuate Na(+)/Ca(2+) exchange, participating in excitation/contraction coupling. The contractile responses in the presence of adrenaline were, however, similar in both high and low K(+) concentrations when increases in extracellular Ca(2+) were applied to increase the demand on excitation/contraction coupling. The possibilities that adrenaline counteracts the effects of high [K(+)] via the sarcoplasmic reticulum or sarcolemmal Na(+)/K(+)-ATPase were examined by inhibiting the sarcoplasmic reticulum with ryanodine (10 micromol l(−1)) or Na(+)/K(+)-ATPase with ouabain (0.25 or 3 mmol l(−)). No evidence to support either of these possibilities was found. Adrenaline did not protect all aspects of excitation/contraction coupling because the maximal frequency giving regular twitches was lower at 10 mmol l(−1) K(+) than at 2.5 mmol l(−1) K(+).

Atrioventricular block in low potassium and K dependence of the nodal resting potential

1986 ◽  
Vol 64 (5) ◽  
pp. 531-538 ◽  
Author(s):  
E. Ruiz-Ceretti ◽  
A. Ponce Zumino
Keyword(s):  
Conduction Block ◽  
Resting Potential ◽  
Long Term Effects ◽  
Progressive Decline ◽  
Outward Currents ◽  
Low Potassium ◽  
Middle Node ◽  
Low K ◽  
Maximum Rate Of Rise

A progressive conduction block leading to atrioventricular dissociation develops in perfused rabbit hearts within 20–30 min of exposure to Krebs containing 0.5 mM potassium (low K). A decrease in potassium permeability resulting in membrane depolarization (as seen in Purkinje fibers) could be responsible for the loss of excitability in nodal cells. We investigated the K dependence of the resting potential and the long-term effects of low K perfusion on the resting and action potentials of nodal cells in rabbit hearts. The resting potential of atrial, atrionodal, and nodal cells varied by 5 2, 41, and 34 mV per decade of change in Ko within the range of 5–50 mM K. Hyperpolarization of the resting membrane, a progressive decline in action potential amplitude, and a decrease in maximum rate of rise were observed in nodal fibers when exposed to low K. Loss of propagated activity occurred in the middle node within 20–30 min while the cells remained hyperpolarized. There was no evidence of electrogenic Na extrusion and it seems that the low nodal resting potential results from a high resting PNa/PK permeability ratio. The early decrease in rate of rise in low K probably reflects an increase in K-dependent outward currents, whereas the progressive deterioration and final loss of conducted electrical activity may result from an accumulation of internal Na and Ca overload produced by low K inhibition of the Na pump.

scholarly journals Changes in Membrane Properties of Chick Embryonic Hearts during Development

1972 ◽  
Vol 60 (4) ◽  
pp. 430-453 ◽  
Author(s):  
Nick Sperelakis ◽  
K. Shigenobu
Keyword(s):  
Action Potential ◽  
Input Resistance ◽  
Membrane Properties ◽  
Resting Potential ◽  
Lower Sensitivity ◽  
Na Channels ◽  
Electrophysiological Properties ◽  
Ventricular Cells ◽  
High K ◽  
Pacemaker Potentials

The electrophysiological properties of embryonic chick hearts (ventricles) change during development; the largest changes occur between days 2 and 8. Resting potential (Em) and peak overshoot potential (+Emax) increase, respectively, from -35 mv and +11 mv at day 2 to -70 mv and +28 mv at days 12–21. Action potential duration does not change significantly. Maximum rate of rise of the action potential (+Vmax) increases from about 20 v/sec at days 2–3 to 150 v/sec at days 18–21; + Vmax of young cells is not greatly increased by applied hyperpolarizing current pulses. In resting Em vs. log [K+]o curves, the slope at high K+ is lower in young hearts (e.g. 30 mv/decade) than the 50–60 mv/decade obtained in old hearts, but the extrapolated [K+]i values (125–140 mM) are almost as high. Input resistance is much higher in young hearts (13 MΩ at day 2 vs. 4.5 MΩ at days 8–21), suggesting that the membrane resistivity (Rm) is higher. The ratio of permeabilities, PNa/PK, is high (about 0.2) in young hearts, due to a low PK, and decreases during ontogeny (to about 0.05). The low K+ conductance (gK) in young hearts accounts for the greater incidence of hyperpolarizing afterpotentials and pacemaker potentials, the lower sensitivity (with respect to loss of excitability) to elevation of [K+]o, and the higher chronaxie. Acetylcholine does not increase gK of young or old ventricular cells. The increase in (Na+, K+)-adenosine triphosphatase (ATPase) activity during development tends to compensate for the increase in gK. +Emax and + Vmax are dependent on [Na+]o in both young and old hearts. However, the Na+ channels in young hearts (2–4 days) are slow, tetrodotoxin (TTX)-insensitive, and activated-inactivated at lower Em. In contrast, the Na+ channels of cells in older hearts (> 8 days) are fast and TTX-sensitive, but they revert back to slow channels when placed in culture.

Membrane permeability during low potassium depolarization in sheep cardiac Purkinje fibers

1979 ◽  
Vol 237 (3) ◽  
pp. C156-C165 ◽  
Author(s):  
C. O. Lee ◽  
H. A. Fozzard
Keyword(s):  
Membrane Potential ◽  
Membrane Permeability ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Low Potassium ◽  
Low K ◽  
Fiber Action ◽  
K Activity

Exposure of sheep Purkinje fibers to low [K]o leads to marked depolarization to a stable potential of about -40 mV. This level is equivalent to the plateau of the Purkinje fiber action potential. The low [K]o depolarization could be prevented by removal of [Na]o and was modified by tetrodotoxin. The membrane potential in the depolarized state was unresponsive to changes in [Cl]o or [Ca]o and it was poorly responsive to changes in [K]o between 0 and 2 mM. Repolarization was induced by decrease in [Na]o with a slope response of 30 mV/10-fold change in [Na]o. Average internal K activity (aK) in the resting state with a [K]o of 5 mM was 121.4 mM for a membrane potential of -80 mV. During low K depolarization aK was 119.7 mM with a membrane potential of -34 mV. The depolarization was therefore due to a change in membrane permeability, with little change in aK. Upon restoration of [K]o the fiber repolarized to values transiently more negative than the prior resting potential. These transient potentials were more negative than the K equilibrium potential (VK), if it is calculated assuming a uniform [K]o. The hyperpolarization was reduced by ouabain [10(-6)] or by low [Ca]o.

Unidirectional flux ratio for potassium ions in depolarized frog skeletal muscle

1981 ◽  
Vol 241 (1) ◽  
pp. C68-C75 ◽  
Author(s):  
B. C. Spalding ◽  
O. Senyk ◽  
J. G. Swift ◽  
P. Horowicz
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Flux Ratio ◽  
External Solution ◽  
Resting Potential ◽  
Frog Skeletal Muscle ◽  
High K ◽  
Sigmoidal Curve ◽  
K Concentration ◽  
Low K

Small bundles of frog skeletal muscle fibers were loaded with 305 mM K+ and 120 mM Cl-, and 42K+ tracer efflux and influx were measured as a function of external K+ concentration ([K+]o) at a resting potential of -2 mV. As [K+]o was lowered from 305 mM, efflux decreased along a markedly sigmoidal curve, reaching a constant nonzero value at low [K+]o. Influx varied linearly with [K+]o at low [K+]o and more steeply at higher [K+]o. The ratio of influx to efflux was described by the equation: influx/efflux = exp[-n(V - VK)F/RT] with n = 2 at high [K+]o, but the ratio approached this equation with n = 1 at low [K+]o. Efflux did not depend on [K+]o when the membrane potential was raised to +36 mV, whereas at low [K+]o decreasing the membrane potential to -19 mV further activated the efflux. The results are discussed in terms of an inwardly rectifying potassium channel with two or more activating sites within the membrane that bind K+ and are accessible from the external solution.

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