scholarly journals Analysis of K Inactivation and TEA Action in the Supramedullary Cells of Puffer

1966 ◽  
Vol 49 (4) ◽  
pp. 629-640 ◽  
Author(s):  
Shigehiro Nakajima
Keyword(s):  
Steady State ◽  
Giant Axon ◽  
Ringer Solution ◽  
Slow Phase ◽  
Rapid Phase ◽  
Inactivation Curve ◽  
Voltage Clamp Condition ◽  
Clamp Condition ◽  
Steady State Levels ◽  
Na Inactivation

Under the voltage clamp condition, the K inactivation was analyzed in cells bathed in the isosmotic KCl Lophius-Ringer solution. After conditioning hyperpolarization, the cells respond to depolarizations with increased K permeability, which in turn is decreased during maintained depolarizations. The steady-state levels of the K inactivation as a function of the membrane potential are related by an S-shaped curve similar to that which describes the steady-state Na inactivation in the squid giant axon. TEA reduced the K conductance by a factor which is independent of the potential, and without a shift of the inactivation curve along the voltage axis. The rapid phase of the K activation is less susceptible to TEA than the slow phase of the K activation. Hyperpolarizing steps remove the K inactivation, the rate of the removal being faster the larger the hyperpolarization from the standard potential of about -60 mv.

Characterization of zinc uptake and its regulation by arachidonic acid in fetal type II pneumocytes

1995 ◽  
Vol 269 (1) ◽  
pp. L71-L77
Author(s):  
T. J. Ong ◽  
P. J. Kemp ◽  
R. E. Oliver ◽  
H. J. McArdle
Keyword(s):  
Arachidonic Acid ◽  
Steady State ◽  
Unsaturated Fatty Acids ◽  
Maximum Velocity ◽  
Zinc Uptake ◽  
Hill Coefficient ◽  
Slow Phase ◽  
Type Ii ◽  
Rapid Phase ◽  
Type Ii Pneumocytes

In freshly isolated fetal guinea pig type II pneumocytes, zinc uptake is time and temperature dependent. Two pathways of uptake exist, resulting in a rapid phase that reaches a steady state within 30 s and a slower linear phase that does not attain a steady state within 60 min. Both processes exhibit saturation kinetics. The rapid phase has a maximal zinc uptake of 60.7 +/- 9.3 pmol.10(6) cells-1.30 s-1 and an apparent affinity (Kt) of 13.7 +/- 5.4 microM. The maximum velocity of uptake (Vmax) of the slower phase is 24.6 +/- 1.9 pmol.10(6) cells-1.min-1 with a Kt of 22.0 +/- 3.6 microM. Epinephrine, terbutaline, dibutyryl adenosine 3',5'-cyclic monophosphate, and dexamethasone have no significant effect on zinc uptake, while arachidonic acid (AA) stimulates. Dose-response data of AA-stimulated zinc uptake gives an apparent K0.5 of 0.42 +/- 0.01 microM and a Hill coefficient of 1. The maximal uptake in the rapid phase is significantly increased to 146.8 +/- 12.4 pmol.10(6) cells-1.30 s-1 and in the slow phase, the Vmax for zinc uptake is also significantly increased to 33.0 +/- 1.8 pmol.10(6) cells-1.min-1 by 10 microM AA. However, the Kt values in both processes remain unchanged after AA stimulation. The effect is not mediated by either leukotrienes or prostaglandins but can be mimicked by other unsaturated fatty acids.

SR Ca loading in cardiac muscle preparations based on rapid-cooling contractures

1989 ◽  
Vol 256 (1) ◽  
pp. C109-C120 ◽  
Author(s):  
D. M. Bers
Keyword(s):  
Steady State ◽  
Guinea Pig ◽  
Slow Phase ◽  
Rapid Cooling ◽  
Relative Index ◽  
Steady State Levels ◽  
Sarcolemmal Transport ◽  
Rat Ventricle ◽  
Ca Sensitivity ◽  
Rabbit Atrium

The influence of rest periods on twitches and rapid-cooling contractures (RCCs) was examined in trabeculae from rabbit, rat, guinea pig, and frog ventricle and rabbit atrium. RCCs were used as a relative index of sarcoplasmic reticulum (SR) Ca content. After increasing rest duration, rabbit and guinea pig ventricles exhibit a decline of both twitch force and RCC force (rest decay). When stimulation is resumed, both twitches and RCCs recover to steady-state levels. The SR (and cells) in these tissues may lose Ca during quiescence and become reloaded with progressive stimulation. Rat ventricle and rabbit atrium exhibited an increase in both twitch and RCC tension as a function of rest duration (rest potentiation). Resumption of stimulation resulted in parallel declines of both twitch and RCC tension approaching steady state. Thus stimulation in rat ventricle and rabbit atrium may lead to a net Ca loss from the SR (and the cell) and quiescence may lead to replenishment of cellular Ca. This major difference in Ca metabolism in mammalian cardiac muscles might be due to a fundamental difference in SR properties or, alternatively, different sarcolemmal transport properties (e.g., action potential configuration, Na-pump). After long rest intervals in rabbit and guinea pig ventricle, RCCs return toward their steady-state value in considerably fewer beats than does twitch tension. This implies that something other than SR refilling is responsible for the slow phase of twitch recovery after rest. In rabbit ventricle increasing frequency or extracellular Ca concentration ([Ca]o) generally increases both twitch and RCC tension. However, decreasing [Ca]o (to 0.2 mM) does not decrease RCCs much despite a dramatic decline in twitch tension (suggesting low twitch tension despite a loaded SR). Rapid rewarming during an RCC usually results in a transient rise in tension (or rewarming "spike"), which is due to a warming-induced increase in myofilament Ca sensitivity. Differences in rewarming spikes among the tissues studied suggest differences in temperature effects on myofilament Ca sensitivity.

scholarly journals The pentose phosphate pathway of glucose metabolism. Enzyme profiles and transient and steady-state content of intermediates of alternative pathways of glucose metabolism in Krebs ascites cells

1969 ◽  
Vol 115 (5) ◽  
pp. 1009-1029 ◽  
Author(s):  
K. A. Gumaa ◽  
Patricia McLean
Keyword(s):  
Steady State ◽  
Glucose Metabolism ◽  
Pentose Phosphate Pathway ◽  
Formation Control ◽  
Pentose Phosphate ◽  
Mass Action ◽  
Slow Phase ◽  
Soluble Enzyme ◽  
Rapid Phase ◽  
Glucose 6 Phosphate Dehydrogenase

1. The pentose phosphate pathway in Krebs ascites cells was investigated for regulatory reactions. For comparison, the glycolytic pathway was studied simultaneously. 2. Activities of the pentose phosphate pathway enzymes were low in contrast with those of the enzymes of glycolysis. The Km values of glucose 6-phosphate dehydrogenase for both substrate and cofactor were about four times the reported upper limit for the enzyme from normal tissues. Fructose 1,6-diphosphate and NADPH competitively inhibited 6-phosphogluconate dehydrogenase. 3. About 28% of the hexokinase activity was in the particulate fraction of the cells. The soluble enzyme was inhibited by fructose 1,6-diphosphate and ribose 5-phosphate, but not by 3-phosphoglycerate. The behaviour of the partially purified soluble enzyme in vitro in a system simulating the concentrations of ATP, glucose 6-phosphate and Pi found in vivo is reported. 4. Kinetics of metabolite accumulation during the transient state after the addition of glucose to the cells indicated two phases of glucose phosphorylation, an initial rapid phase followed abruptly by a slow phase extending into the steady state. 5. Of the pentose phosphate pathway intermediates, accumulation of 6-phosphogluconate, sedoheptulose 7-phosphate and fructose 6-phosphate paralleled the accumulation of glucose 6-phosphate. Erythrose 4-phosphate reached the steady-state concentration by 2min., whereas the pentose phosphates accumulated linearly. 6. The mass-action ratios of the pentose phosphate pathway reactions were calculated. The transketolase reaction was at equilibrium by 30sec. and then progressively shifted away from equilibrium towards the steady-state ratio. The glucose 6-phosphate dehydrogenase was far from equilibrium at all times. 7. Investigation of the flux of [14C]glucose carbon confirmed the existence of an operative pentose phosphate pathway in ascites cells, contributing 1% of the total flux in control cells and 10% in cells treated with phenazine methosulphate. 8. The pentose phosphate formed by way of the direct oxidative route and estimated from the 14CO2 yields represented 20% of the total accumulated pentose phosphate, the other 80% being formed by the non-oxidative reactions of the pentose phosphate pathway. 9. The pentose phosphate pathway appears to function as two separate pathways, both operating towards pentose phosphate formation. Control of the two pathways is discussed.

scholarly journals Two Inward Currents in Frog Atrial Muscle

1971 ◽  
Vol 58 (5) ◽  
pp. 523-543 ◽  
Author(s):  
Merrill Tarr
Keyword(s):  
Action Potential ◽  
Voltage Clamp ◽  
Ionic Currents ◽  
Ringer Solution ◽  
Slow Inward Current ◽  
Slow Phase ◽  
Free Solution ◽  
Rapid Phase ◽  
Inward Current ◽  
Atrial Tissue

The double sucrose-gap voltage-clamp technique was applied to frog atrial tissue to investigate the ionic currents responsible for the action potential in this tissue. Membrane depolarization elicited two distinct components of inward current when the test node was exposed to normal Ringer solution: a fast inward current and a slow inward current. The fast inward current appeared to be carried by sodium ions, since it was rapidly abolished by exposure of the fiber to Na+-free solution or tetrodotoxin but persisted on exposure to Ca++-free solution. In contrast, in the majority of the preparations the slow inward current appeared to be primarily carried by calcium ions, since it was abolished on exposure of the fiber to Ca++-free solution but persisted on exposure to Na+-free solution. Action potential data supported the voltage-clamp findings. The normal action potential shows two distinct components in the upstroke phase: an initial rapid phase of depolarization followed by a slower phase of depolarization reaching the peak of the action potential. Abolition of the fast inward current resulted in abolition of the initial rapid phase of depolarization. Abolition of the slow inward current resulted in abolition of the slow phase of depolarization. These data support the hypothesis that two distinct and different ionic mechanisms contribute to the upstroke phase of the action potential in frog atrial tissue.

scholarly journals Dissociation of Calcium Transients and Force Development following a Change in Stimulation Frequency in Isolated Rabbit Myocardium

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Kaylan M. Haizlip ◽  
Nima Milani-Nejad ◽  
Lucia Brunello ◽  
Kenneth D. Varian ◽  
Jessica L. Slabaugh ◽  
...  
Keyword(s):  
Steady State ◽  
Late Phase ◽  
Force Production ◽  
Calcium Transient ◽  
Stimulation Frequency ◽  
Calcium Handling ◽  
Slow Phase ◽  
Rapid Phase ◽  
Force Development ◽  
Time To Peak

As the heart transitions from one exercise intensity to another, changes in cardiac output occur, which are modulated by alterations in force development and calcium handling. Although the steady-state force-calcium relationship at various heart rates is well investigated, regulation of these processes during transitions in heart rate is poorly understood. In isolated right ventricular muscle preparations from the rabbit, we investigated the beat-to-beat alterations in force and calcium during the transition from one stimulation frequency to another, using contractile assessments and confocal microscopy. We show that a change in steady-state conditions occurs in multiple phases: a rapid phase, which is characterized by a fast change in force production mirrored by a change in calcium transient amplitude, and a slow phase, which follows the rapid phase and occurs as the muscle proceeds to stabilize at the new frequency. This second/late phase is characterized by a quantitative dissociation between the calcium transient amplitude and developed force. Twitch timing kinetics, such as time to peak tension and 50% relaxation rate, reached steady-state well before force development and calcium transient amplitude. The dynamic relationship between force and calcium upon a switch in stimulation frequency unveils the dynamic involvement of myofilament-based properties in frequency-dependent activation.

Activation, inactivation and recovery in the sodium channels of the squid giant axon dialysed with different solutions

1992 ◽  
Vol 337 (1282) ◽  
pp. 471-484 ◽  
Keyword(s):  
Steady State ◽  
Permeability Coefficient ◽  
Reversal Potential ◽  
Giant Axon ◽  
Inactivation Curve ◽  
Gating Charge ◽  
Recovery From Inactivation ◽  
Sodium System ◽  
Steady State Inactivation ◽  
Open States

Comparisons were made between families of ion currents recorded in voltage-clamped squid axons dialysed with 20 mM NaF and 330 mM CsF or TMAF, and bathed in a solution in which four fifths of the Na was replaced by Tris. The permeability coefficient P Na,fast for the fast-inactivating current in the initial open state was calculated as a function of test potential from the size of the initial peak of I Na . The permeability coefficient P Na,non for the non-inactivating open state was calculated from the steady-state I Na that persisted until the end of the test pulse. Dialysis with TMA had no direct effect on the Qv curve for gating charge. The reversal potential for I Na,non was always lower than that for I Na,fast , the mean difference being about — 9 mV when dialysing with Cs, but only about — 1 mV with TMA. Except close to threshold, P Na,fast was roughly halved by dialysis with TMA as compared with Cs, but P Na,non was substantially increased. The time constant τ h for inactivation of the sodium system was slightly increased during dialysis with TMA in place of Cs, and there were small shifts in the steady-state inactivation curve, but the rate of recovery from inactivation was not measurably altered. The flattening off of the τ h curve at increasingly positive test potentials corresponded to a steady reduction of the apparent inactivation charge until a value of about 0.2 e was reached for pulses to 100 mV. The instantaneous I-V relationship in the steady state was also investigated. The results have a useful bearing on the effects of dialysis with TMA, on the differences between the initial and steady open states of the sodium channel, and on the relative voltage-dependences of the transitions in each direction between the resting and inactivated states.

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