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Biomedical subjects

A Yatani

Publications and source records attributed to A Yatani.

At least 127 records · Page 7Linked to original sources
PubMed1984

The effects of caffeine on the electrical properties of isolated, single rat ventricular cells.

The effects of caffeine on ionic currents in isolated, single cells from rat ventricles were compared with the effects of adrenaline. In current-clamp experiments, caffeine (1.0 to 10.0 mM) increased both the height of the plateau and the duration of the action potential. Both caffeine and adrenaline increased the amplitude and duration of the slow responses. Voltage-clamp experiments reveal that the repolarization phase of the action potential in isolated cells is determined mainly by the slow inward current (Is), which has voltage-dependent kinetics similar to the Is in intact cardiac tissue: No evidence of a time-dependent outward current (Ix), or a hyperpolarization-induced inward current (Ih) or (If) was found, although a time-independent background current (Ik1) was observed. Caffeine increased the amplitude of Is, but did not change its time course, its voltage dependency (of steady-state inactivation and activation), or its apparent reversal potential. Ik1 is not affected by the caffeine. The results indicated that the effects of caffeine were nearly identical to those of adrenaline. The effects of caffeine on the electrical properties of single cells from rat ventricles derive chiefly from its action on Is channels.

Action Potentials↗
PubMed1984

Permeability to various cations of the voltage-dependent sodium channel of rat single heart cells.

The permeability to various cations of the voltage-dependent sodium channel of rat single heart cells has been studied under the current or voltage clamp conditions. The cells, dispersed by collagenase treatment, were perfused internally using a suction pipette technique. The permeability sequence, estimated from the effects of various cations on the maximum rate of rise of action potential or from either the peak amplitude or the reversal potential of the inward current was Na+ greater than Li+ greater than hydrazine greater than guanidine greater than formamidine greater than hydroxylamine greater than methylguanidine greater than monomethylamine. The ionic permeability of a compound was markedly diminished by methylation. All inorganic and organic cation currents were reduced in the presence of tetrodotoxin, a specific Na+ channel blocker. It would appear that the ionic selectivity of the sodium channel of rat single heart cells is similar to the selectivity in the squid axon and of that in the myelinated nerve of the frog.

Action Potentials↗
PubMed1983

Recovery of Ca currents from inactivation: the roles of Ca influx, membrane potential, and cellular metabolism.

Ca currents were examined with regard to their recovery from inactivation. The experiments were done on isolated nerve cell bodies of Helix aspersa using a combined suction pipet , microelectrode method for voltage clamp, and internal perfusion. Ca currents were separated by suppressing K and Na currents. The time course of recovery was determined by applying a test pulse at intervals ranging from 1 msec to 20 sec after prepulses varying from 20 to 3000 msec in duration. Each pair of pulses was preceded by a control pulse to ensure that the Ca currents had recovered before the next test pair was applied. Ba and Ca currents were compared and the effects of intracellular perfusion with EGTA, ATP, and vanadate were examined. Ba currents recovered in two stages and this time course was well fit by a sum of two exponentials with amplitudes and time constants given by A1 and tau 1 for the fast component and A2 and tau 2 for the slow component. In Ba the time constants were unchanged when prepulse durations were prolonged from 70 to 700 msec, although the initial amplitudes A1 and A2, particularly A2, were increased. Comparable influxes of Ca during the prepulse caused much more inactivation, but interestingly the recovery occurred at the same rate. The time course of Ca current recovery was also fit by a sum of two exponentials, the time constants of which were both smaller than the time constants of Ba current recovery. However, the time constants of Ca current recovery were increased markedly when prepulse durations were prolonged. Increasing the extracellular Ca concentration had a similar effect. Increasing the Ba influx had no effect on the recovery time constants, and the Ba results are consistent with reversible inactivation gating of potential-dependent membrane Ca channels. The Ca results show that Ca influx enhances inactivation. Intracellular perfusion with EGTA resulted in less inactivation in the cast of Ca but it had no effect on Ba currents. Intracellular ATP increased the rate of recovery of Ca currents, and intracellular vanadate inhibited recovery. It is concluded that recovery of Ca channels depends upon both Ca influx and membrane potential and is modulated by agents which affect Ca metabolism.

Adenosine Triphosphate↗
PubMed1983

Voltage-dependent activation of potassium current in Helix neurones by endogenous cellular calcium.

1. The effect of endogenous Ca on potential-dependent K current IKD, was examined in identifiable neurones of Helix aspersa. The suction pipette method of internal perfusion was used along with a combined voltage-clamp method in which the membrane potential was measured by a separate glass micro-electrode and the current was passed by the suction pipette. Activation of the potential-dependent A current, IA, was prevented by using holding potentials of -40 mV where IA is inactivated and by the addition of the A-current blocker 4-aminopyridine. Activation of K currents by transmembrane Ca current, IKCa, was suppressed by Co substitution for Ca ion extracellularly. 2. Under these conditions, IKD rose to a peak value and then subsided to a steady level. The current-voltage (I-V) relationship for peak IKD had an upward bump at about +50 mV that gave it an S-shape. The I-V curve for steady IKD rose continuously. Peak and steady IKD were reduced by perfusing with EGTA or F ions intracellularly. The EGTA effect occurred at intracellular Ca activity levels below 10(-7) M. Increases in the concentration of EGTAi at constant Cai had no additional effect; however, recovery experiments do not allow us to rule out some direct action of EGTA on IKD. 3. Prolonged extracellular perfusion with Co-substituted solutions also reduced IKD and the effects occurred more quickly when the solutions were made hypertonic or caffeine was added to them. The peak transient was abolished, and the small remaining steady IKD (about 5-10% of normal peak IKD) was blocked by tetraethylammonium. IKD could be restored by the temporary reintroduction of Ca in the extracellular solution. 4. The S-shape of the peak I-V relationship for IKD may be due to Ca released from an endogenous site by membrane depolarization. The reduction of steady and peak IKD to very low values by Ca chelators or prolonged perfusion with Ca-free solutions indicates that Cai is important for activation of these K channels. 5. Three cellular structures were identified in electron micrographs of freeze-fractured neurones that could be involved in potential-dependent endogenous Ca release. These were a restricted extracellularly space, an intracellular membrane system of endoplasmic reticulum that may be fused to the internal face of the plasma membrane (the subsurface cisterns of Henkart & Nelson, 1979), and intracellular vesicles that also may be fused to the plasma membrane.

Animals↗
PubMed1983

The effect of extracellular low pH on the plateau current in isolated, single rat ventricular cells--a voltage clamp study.

When the electrical properties of single, isolated, rat ventricular cells at low pH were examined, the amplitude of the action potential and its duration were found to decrease at low pH (less than 5.5). In voltage clamp experiments, the low pH depressed Ia and slowed the inactivation process, yet the outward currents reflecting the plateau range of the action potential were not affected. The I-V curve of Is shifted to less negative potentials at low pH. Similar results were obtained in ISr and IBa at low pH. The alteration of the action potential of single ventricular cells at low pH is attributed to the suppression of Is. The mechanism of this reduction of Is might be due to the presence of a surface potential capable of affecting gating and permeation mechanisms of Is channel or to the protonation of some acidic group that must be ionized for the Is channel to function normally.

Action Potentials↗
PubMed1982

After effects of perfusion with glucose-insulin-potassium solution on the membrane current and tension components of frog atrial muscle.

As glucose-insulin-potassium solution (GIK) has been used as clinical cardioplegia during open heart surgery, we studied the fundamental effects of GIK on the electrical and mechanical activities of the bullfrog atrial muscle under voltage clamped and unclamped conditions by the double sucrose-gap method. GIK produced an immediate disappearance of the action potential and twitch tension with pronounced depolarization accompanied by transient contracture. Reperfusion with normal Ringer's solution after GIK perfusion (30-180 min) resulted in recovery of the action potential, with an initial lengthening followed by a sustained shortening in duration. Recovery of twitch tension was incomplete, and perfusion with GIK for a longer period caused stronger suppression. Voltage clamp studies revealed that after removal of GIK, the slow inward current (Is) and Is-dependent tension were markedly depressed, while the delayed outward current (Ix) was augmented. The fast inward current (INaf), background current (Ik1), and Is-independent tension gradually recovered to the control levels. Perfusion with low Ca Ringer's solution or verapamil Ringer's solution for 10 min at the initial reperfusion phase significantly improved the recovery of Is and the Is-dependent tension. These results indicate that the after-effects of GIK are mainly governed by Ca influx at the initial reperfusion phase. Therefore, a lowering of the Ca influx in this period is expected to produce a beneficial effect on cardiac function after GIK treatment.

Action Potentials↗
PubMed1981

Interaction of adenosine and acetylcholine on the bullfrog atrium.

As adenosine has a potent stabilizing action on catecholamine stimulation in the myocardium, the mode of interaction of adenosine and acetylcholine (ACh) was studied with regard to the membrane potential, current and tension components of the bullfrog atrium, using the single or double-sucrose gap method. Adenosine (10(-4)-3 x 10(-3)M) augmented the twitch contraction in the presence of ACh(10(-9)-5 x 10(-7)M) by lengthening the duration of the action potential. The dose-tension response curve for ACh was modified by adenosine, producing a rise of the inhibitory threshold of ACh, and the modification showed a non-competitive interaction of these compounds. Under the voltage clamp, ACh-induced steady current (IACh) was inhibited by adenosine non-competitively. The known inhibition of slow inward current (Is) by ACh was enhanced by adenosine, while the delayed outward current (Ix) was markedly suppressed. Is-dependent and -independent tension components were both inhibited by adenosine, thereby suggesting a decrease in intracellular concentrations of calcium. The potent suppression of IACh and Ix induced by adenosine, however, appeared to mitigate the inhibitory action of ACh on the action potential and twitch contraction.

Acetylcholine↗
PubMed1980

Antagonistic action of alpha- and beta-agonists on the bullfrog atrium.

Action of alpha- and beta-agonists on the membrane potential, current and tension components on the bullfrog atrial muscle were studied by means of the single or double sucrose-gap technique. Isoproterenol (10(-9)-10(-5) M) as well as adrenaline (10(-7)-10(-4) M) produced a dose-dependent positive inotropic effect, while methoxamine (10(-8)-10(-4) M) and phenylephrine (10(-8)-10(-3) M) with propranolol (10(-6) M) elicited a negative inotropic effect. The positive inotropic effect was accompanied by slight hyperpolarization and marked increase of over-shoot and plateau level of action potential, and the negative inotropic effect, by opposite changes. Under voltage clamp, isoproterenol and adrenaline produced enhancement of slow inward current (Is), delayed outward current (Ix) and Is-dependent phasic tension, while Is-independent tonic tension was inhibited. Contrarily, methoxamine and phenylephrine depressed these currents and elicited beta-antagonistic inotropic actions, especially when isoproterenol was present. Specific feature of alpha-agonist action in the presence of isoproterenol was an inward shift of the semi-steady I-V relationship. It is thus suggested that, in the bullfrog atrium, alpha-agonists produce a strong beta-receptor blocking action and an inward shift of the background current. A possible relationship between the latter effect and inhibition of the Na-K pump is also suggested.

Action Potentials↗
PubMed1979

Interaction between caffeine and adenosine on the membrane current and tension component in the bullfrog atrial muscle.

Antagonistic action of caffeine and adenosine were studied at the membrane current and tension component levels in myocardium of the bullfrog atrium, mainly under voltage clamp using the double sucrose-gap method. Caffeine (1-5 mM) produced marked augmentation of the phasic and tonic tensions as well as slow inward current (Is). At higher concentrations it elicited an increase of the delayed outward current (Ix). The augmentation of Is was principally due to increase of the limiting conductance (gs), while the activation and inactivation variables (dinfinity, finfinity) were not changed significantly. The dose-tension response curve for caffeine, which appeared sigmoidal, was notably lowered in the presence of adenosine (1-3 mM), indicating a competitive type of inhibition. Adenosine, in the presence of caffeine, exerted a narcotic-like action by inhibiting all of the membrane currents (INaf, Is, Ix and background inward current, Ib) and tension components (ICa-dependent and independent tensions). The inhibition of Is was due to a decrease of gs and no appreciable change was observed in dinfinity and finfinity. These results suggest that adenosine has a strong stabilizing action on the myocardium, especially when the heart muscle activity is accelerated by increased cyclic AMP.

Action Potentials↗
PubMed1978

Effect of low temperature on the membrane currents and tension components of bullfrog atrial muscle.

In order to clarify the nature of inotropic action of low temperature, the effects of cooling on the membrane currents and tension components were studied on the bullfrog atrial muscle under voltage clamped and unclamped conditions with double gap method. Cooling (in between 35 degrees-7 degrees C) produced an increase of overshoot and a prolongation of the action potential accompanied by a slight depolarization of the membrane, a decrease of basal tension and an increase of twitch contraction. Under voltage clamp, a marked augmentation of contraction also occurred despite a decrease of basal tension, suggesting that the inotropic effect of cooling is not merely dependent on the prolongation of action potential. When the components of membrane current and tension were isolated in modified Ringer solutions, it became clear that ICa and ICa -dependent tension markedly increased at low temperature, while all other currents (INaf, INas, IK1 Ix) and ICa-independent tension decreased. Leaky membrane current (I1) for hyperpolarizing pulses also diminished. Temperature coefficient (Q10) of the ICa-independent tension component was 1.2-1.5 between 7 degrees C and 17 degrees C, while that of ICa-dependent tension varied depending on depolarization voltages. These data were discussed in relation to possible alteration of Ca concentration at outer and inner layers of the membrane which may depend on temperature.

Action Potentials↗
PubMed1978

Nature of catecholamine-like actions of ATP and other energy rich nucleotides on the bullfrog atrial muscle.

The nature of the inotropic actions of exogeneously applied ATP and related compounds (AMP-PNP, GTP, GMP and guanosine) was studied in comparison with that of adrenaline on the bullfrog atrial muscle under voltage clamped and unclamped conditions with the double-gap method. ATP and GTP (10(-6-) - 10(-3) M) produced an immediate positive inotropic effect similar to that achieved with adrenaline. Dose-response curves of these drugs fitted the theoretical dose-response relations, but the curves of ATP and GTP were not significantly altered by propranolol. Under voltage clamped conditions, ATP, AMP-PNP (non-hydrolyzable analogue of ATP) and GTP augmentated the calcium inward current (ICa), ICa-dependent tension and the delayed outward current (Ix) as adrenaline. On the other hand, GMP and guanosine, which have a purine-ribose base but not a high energy phosphate bond, produced a negative inotropic effect, and depressed the Ix as adenosine. All these nucleotides and nucleosides inhibited the ICa-independent tonic tension. The facts that GTP and AMP-PNP showed the same effect as ATP indicated that neither the energy liberation from the phosphate bond nor the substrate for cyclic AMP formation is involved in their positive inotropic effects. It is proposed that the energy rich nucleotides modulate the adenylate cyclase activity, being mediated by some receptor located at the outer surface of the membrane other than beta-adrenergic receptor.

Adenosine Triphosphate↗
PubMed1978

Stabilizing effects of adenosine on the membrane currents and tension components of the bullfrog atrium.

The effects of exogenously applied adenosine on the membrane potentials, currents and tension components of the bullfrog double sucrose-gap method. Adenosine above 10(-3)M produced a prolongation of action potential accompanied by a slight augmentation of contraction which was followed by a sustained depression. The recovery was slow. Under voltage clamp conditions, adenosine merely produced a negative inotropic effect depressing Ica-dependent and -independent tensions. In the membrane currents, Inaf, Is(Ica), Ix and background current (Ib) were all depressed. In the presence of adrenaline, the increased Is, Ix and contraction were inhibited by adenosine in a lower dose (10(-5) -10 (-3) M), and the inhibition of Is and Ica-dependent tension were more prominent in the presence of than in the absence of adrenaline. Under the effect of ATP, which has a catecholamine-like action, similar selective inhibitions were observed. It was concluded that adenosine has a sustained stabilizing action on the myocardium to survive, especially in the presence of adrenaline, by depressing the augmented Ica and contraction.

Adenosine↗
PubMed1977

An analysis of the action of ATP and related compounds on membrane current and tension components in bullfrog atrial muscle.

The effect of adenosine compounds (ATP, ADP, AMP and adenosine) on membrane potential, current and contractile tension on the bullfrog atrium were studied under voltage clamped and unclamped conditions. The compounds produced immediate positive and late negative inotropic effects in unclamped conditions. The positive inotropic effect and the potency of drugs appeared less marked in the order of ATP, ADP, AMP, and adenosine. Under voltage clamped conditions, only the energy rich compounds, ATP and ADP, produced an enhancement of calcium inward current (Ica) and Ica-dependent phasic tension, while AMP and adenosine elicited a negative inotropic effect. The delayed outward current was initially depressed but later augmented epecially in case of ATP and ADP where Ica was enhanced. All adenosine compounds, however, inhibited the Ica-independent tonic tension. This effect, appearing nonspecific, was ascribable to the action of common structure of these compounds, purine-riboside moiety.

Adenine Nucleotides↗