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Biomedical subjects

H Kotake

Publications and source records attributed to H Kotake.

At least 163 records · Page 9Linked to original sources
PubMed1986

Studies on the bradycardia induced by aprindine in rabbit sinoatrial node cells.

The effects of aprindine (1 X 10(-7) to 4 X 10(-6) M) were examined on membrane potential and current of rabbit sinoatrial node by means of conventional microelectrode and double microelectrode voltage clamp methods. Aprindine decreased, in a dose-dependent manner, the spontaneously firing frequency, the maximum rate of depolarization and the action potential amplitude, and prolonged the action potential duration at half-amplitude. The slope of the diastolic depolarization was also reduced by the drug. In the voltage clamp experiment, aprindine reduced the slow inward current (Isi), the time-dependent potassium current (Ik) and the hyperpolarization activated current (Ih). The recovery time constant of Isi was prolonged by aprindine, while the kinetics of Ik was not altered. It is indicated that aprindine does not have an effect on a specific conductance or a single current system, but that the drug exerts an inhibitory effect on the electrical activity of sinoatrial node.

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PubMed1986

Study on bradycardia induced by diltiazem in the rabbit sinoatrial node.

Effects of 3-(acetyloxy)-5-[2-(dimethylamino)ethyl]-2, 3-dihydro-2-(4-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one (diltiazem) on the membrane currents of rabbit sinoatrial node cells were examined using the double microelectrode voltage clamp technique. The transmembrane slow inward current (Isi) was reduced after 0.5 mumol/l diltiazem perfusion and Isi was nearly completely suppressed by 2.2 mumol/l diltiazem. As to the blockade of Isi, diltiazem revealed a dose-dependent fashion. Diltiazem also produced a slight decrease of both the steady-state current during depolarization and the tail current after repolarization in these concentration ranges, while the hyperpolarization activated current (Ih) was not affected significantly. Furthermore, higher concentration of diltiazem (10 mumol/l) decreased the steady-state outward current amplitude during depolarization, implying that diltiazem might reduce the potassium outward current (Ik). It is concluded that diltiazem suppressed Isi in a use-dependent manner, not surprisingly, but the drug exerted an additional effect of a decrease in Ik of sinoatrial node cells.

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PubMed1986

Electrophysiological effect of trapidil on rabbit sinoatrial node cells.

Effects of trapidil on the membrane potentials and currents of rabbit sinoatrial node cells were investigated by means of conventional microelectrode and double microelectrode voltage clamp methods. Trapidil (1 X 10(-4) M) increased the spontaneous firing frequency, the maximum rate of rise, action potential amplitude and the slope of the pacemaker depolarization. Action potential duration was shortened by the drug application. Voltage clamp experiments showed that trapidil increased both the slow inward current (isi) and the potassium outward current (iK). Trapidil fastened the recovery time constant of isi, while the drug did not change the time course of the outward current tail. The hyperpolarization-activated current (ih) was also increased by the drug. The results obtained indicate that at relatively high concentration trapidil produces a positive chronotropic effect on the sinoatrial node cells by mediating an increase in isi, iK and ih.

Animals↗
PubMed1985

Effects of dilazep on the electrophysiological properties of rabbit sinoatrial node cells.

The electrophysiological effect of dilazep (1 X 10(-7) -3 X 10(-6) M), a coronary vasodilator, was examined on rabbit sinoatrial node cells using glass microelectrode and double microelectrode voltage clamp methods. Dilazep exerted a negative chronotropic effect and decreased the maximum rate of depolarization of the upstroke of the action potential and the amplitude of the action potential. The action potential duration at half-amplitude was prolonged after the drug perfusion. The voltage clamp experiment showed that dilazep reduced the slow inward current (Isi), the potassium outward current (IK), and the hyperpolarization-activated current (Ih). The recovery time constant of Isi was also prolonged. In conclusion, it is indicated that dilazep has no specific effect on the current system, but the drug depresses specifically the electrical activity of sinoatrial node cells.

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PubMed1985

Electrophysiological effect of disopyramide on rabbit sinus node cells.

The effects of disopyramide on the membrane potentials and currents of rabbit sinus node cells were studied using the conventional microelectrode and voltage clamp methods. Disopyramide (5 and 10 micrograms/m1) produced a negative chronotropic effect, and decreased the maximum rate of depolarization, the overshoot potential and the maximum diastolic potential. The action potential duration at half-amplitude was prolonged, and the slope of diastolic depolarization was reduced. In the voltage clamp experiments, disopyramide (10 and 50 micrograms/m1) reduced the potassium outward current (IK) without changing its kinetics. Disopyramide reduced the slow inward current Isi and increased the recovery time constant of Isi. The hyperpolarization-activated current (Ih) was also decreased by the drug. From these results, it is concluded that disopyramide has a depressant effect on the electrical activity of sinus node cells by mediating depression of IK, Isi and Ih.

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PubMed1981

Kinetics and rectification of the slow inward current in the rabbit sinoatrial node cell.

The slow inward current (is) in the rabbit sinoatrial node cell was studied by the conventional two-microelectrode voltage clamp technique. When is was measured as the difference between two records obtained before and after blocking is with D 600, the fully activated current (is)-voltage relation was non-linear; the conductance decreased in the negative potential range resulting in an almost constant amplitude of is negative to -10 mV. The degree of steady-state activation was about 1 at -5mV and 0 at -65mV. The recovery time course of is during repolarization was measured by varying the interval between two sequential depolorizing pulses with various holding potentials. The time constant of the exponential recovery time course was about 120 msec at -40 mV and decreased to about 40 msec at -70 mV. The steady-state conductance of is, calculated from the activation and inactivation curves, produced a large hump in the steady-state current voltage relation between -60 and -20 mV, which was not observed in the experiment. When the above kinetics were incorporated, the S-A node model failed to discharge the spontaneous activity. The activation and inactivation curves which can simulate the experimental I-V curve and the action potential were proposed.

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PubMed1980

Slow inward current and its role mediating the chronotropic effect of epinephrine in the rabbit sinoatrial node.

The ionic mechanism underlying the chronotropic effect of epinephrine on the rabbit sinoatrial (S-A) node has been studied. Epinephrine (5.5 X 10(-6) M) increased the spontaneous rate from 206 +/- 25 min-1 to 242 +/- 39 min-1. The effect of epinephrine was reproducible on repetitive applications. Voltage clamp experiments using the two microelectrode technique revealed the following changes in the membrane current: epinephrine (5.5 X 10(-7) M) increased the limiting conductance for the slow inward current (is) by approximately 30% and the potassium current (ik) by about 10%, keeping the kinetics of is and ik constant. From the holding potential of -70 mV the activation of is was observed on step depolarization positive to -60 or -55 mV in both control and epinephrine solution. The hyperpolarization-activated current (ih) was also increased by about 20% at -70 mV, and its time course was slightly accelerated. Participation of is for the chronotropic effect of epinephrine was strongly suggested by the findings that is was partially available positive to -60 mV and that epinephrine could not increase the slope of diastolic depolarization when is was blocked by D 600.

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PubMedDate not supplied

On the mechanism underlying the oscillatory current in cardiac Purkinje fibers.

The mechanism underlying the oscillatory current (Ios) was investigated in sheep cardiac Purkinje fibers with a voltage-clamp technique. The Ios is initiated not only by repolarizing but also by a depolarizing clamp, provided that the preparation is preloaded with calcium by means of a conditioning clamp and that the depolarizing test clamp initiates the slow inward current. The Ios initiated by a depolarizing test clamp is usually smaller and has a longer time to peak than that initiated by a repolarizing clamp to the same potential. Brief depolarizing clamps can be followed by an Ios in fibers preloaded with calcium. The amplitude of Ios diminishes as the interval from the conditioning clamp increases. No Ios is initiated by repolarizing or depolarizing clamps to potentials positive to approximately -30 to -40 mV even when [Na]0 is lowered. If a test clamp is applied at a peak of Ios to potentials less negative than approximately -30 mV, the current disappears. The membrane conductance during the Ios is lower. It is concluded that Ios is initiated indirectly by repolarization and is due to a calcium-triggered release of calcium which may initiate an electrogenic Na-Ca exchange.

Animals↗
PubMedDate not supplied

Effects of enalapril on the exercise capacity and neurohumoral factors during exercise in patients with chronic heart failure.

The effects of enalapril on exercise capacity and neurohumoral factors during exercise were evaluated in 10 patients with heart failure. Echocardiograms and exercise testing with expired gas analysis were performed before and after enalapril. Blood samples were obtained before and after exercise. Both ejection fraction and percent fractional shortening increased with enalapril (p < 0.05). The anaerobic threshold and peak VO2 did not change with enalapril. Epinephrine and norepinephrine levels at peak exercise decreased with enalapril (p < 0.1). Plasma renin both at rest and at peak exercise increased with enalapril (p < 0.1). Angiotensin II was lower after enalapril both at rest and at peak exercise (p < 0.1 and p < 0.05, respectively). Aldosterone was lower after enalapril both at rest and at peak exercise (p < 0.05). Atrial natriuretic peptide (ANP) was lower after enalapril both at rest and at peak exercise. There was no significant correlations between peak VO2 and changes in neurohumoral factors before and after enalapril during exercise. In conclusion, neurohumoral changes with enalapril occurred during exercise even if exercise capacity did not improve. Moreover, the improvement of cardiac function at rest and neurohumoral factors with enalapril did not lead to a change of exercise capacity.

Aged↗
PubMedDate not supplied

Cardiac neurosis: exercise tolerance and the role of sympathetic activity.

To evaluate the cardiovascular and plasma catecholamine responses to dynamic exercise in patients with cardiac neurosis (CN), treadmill testing was performed. Thirty-four patients with CN were chosen for this study based on exercise tolerance and the results were compared with those in 31 patients with organic heart disease and 12 normal subjects. Patients with CN showed an augmentation of cardiovascular and plasma catecholamine responses. The augmentation of the norepinephrine response in patients with CN was not as remarkable as that in patients with organic heart disease. On the other hand, the augmentation of the epinephrine response was greater in patients with CN than in those with organic heart disease. Administration of metoprolol (40 mg/day) for two weeks improved exercise tolerance in patients with CN. We suggest that anxiety augments both sympatho-neural and sympatho-adrenal activity and that it is the symptoms induced by the augmented cardiovascular response which reduce exercise tolerance in patients with CN.

Adult↗
PubMedDate not supplied

Ebstein's anomaly with non-patent ductus arteriosus aneurysm and bradycardiac atrial fibrillation in an 80-year-old man.

An 80-year-old man with Ebstein's anomaly and ductus arteriosus aneurysm is reported. He was admitted with bradycardiac atrial fibrillation and right ventricular failure. For the control of brady-arrhythmia, a permanent pacemaker was implanted. Two-dimensional echocardiogram revealed distal displacement of the septal tricuspid valve. Aortography and computed tomography showed ductus arteriosus aneurysm. This is the first report of the association of Ebstein's anomaly and non-patent ductus arteriosus aneurysm.

Aged↗
PubMedDate not supplied

Effects of guanabenz acetate on the pacemaker activity of rabbit sinoatrial node cells.

The effects of guanabenz acetate on the electrophysiological properties of isolated rabbit sinoatrial node were studied using conventional microelectrode and double-microelectrode voltage clamp methods and were compared with those of clonidine and guanethidine. In spontaneously beating sinoatrial node preparations, guanabenz decreased the heart rate, the maximum rate of rise (Vmax), the action potential amplitude and the rate of diastolic depolarization in a dose-dependent fashion, whereas the action potential duration at 50% repolarization was prolonged. In comparison with clonidine and guanethidine, the inhibitory potency of guanethidine on the heart rate is weaker than that of guanabenz and clonidine. On the current systems, the voltage clamp experiments showed that guanabenz reduced the slow inward current and the time-dependent potassium outward current. These observations indicate that guanabenz acts directly on cardiac tissues and its bradycardic action can be mainly explained by a reduction of delayed current systems.

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