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Biomedical subjects

R Ochi

Publications and source records attributed to R Ochi.

At least 19 recordsLinked to original sources
PubMed1992

Adrenoceptor-mediated effects on calcium channel currents are antagonized by 5'-(N-ethyl)-carboxamido-adenosine in guinea-pig atrial cells.

In guinea-pig atrial myocytes, the effects of the adenosine analogue 5'-(N-ethyl)-carboxamido-adenosine (NECA) in the presence of isoprenaline (ISO) on Ca2+ channel activity were analyzed. Single Ca2+ channel currents were recorded from cell-attached patches by application of several hundred 100 ms depolarizing steps. Under control conditions, burstlike activity of channel openings during some depolarizing steps were followed by variably long periods of quiescence (blank sweeps). During superfusion with ISO (100 nmol/l), ensemble-averaged (mean) current was increased by about 150%. The underlying mechanism was found to be a significant increase in the channel availability, defined as the ratio of current-containing sweeps to the total number of sweeps. In addition, the ISO-induced reduction of blank sweeps was combined with slightly but not significantly higher values of the open probability in the current-containing sweeps. Open time and shut time histograms could be fitted by single and double exponential curves, respectively, which remained rather unaffected in the presence of ISO; accordingly, mean open time and mean shut time of the channel were not significantly changed by ISO. After the addition of NECA (1 mumol/l) in the presence of ISO, the ISO-induced increase in mean current was abolished. This effect of NECA on mean current was due to a reduction of the channel availability and a slight decrease in the open probability. The purinoceptor blocking agent 8-phenyltheophylline (10 mumol/l) antagonized the inhibitory action of NECA on the ISO-induced increase in Ca2+ channel activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1992

[Acid-base balance and contraction of the cardiac muscle].

In cardiac muscle, intracelular pH (pHi) is regulated to close to 7.1, both by membrane transport systems (Na-H and Cl-HCO3 exchange) and intracellular H+ buffers. Internal acidosis depresses the contraction, while alkalosis increases it. Internal proton depresses the contraction even without altering the internal concentration of Ca (Cai). The proton blocks the Ca channels. However, as it releases membrane-bound Ca and the influx of Na via Na-H exchange increases Ca influx through Na-Ca exchange, pHi decrease is often accompanied by the Cai increases. The internal proton also affects the uptake and release of sarcoplasmic reticulum, Ca binding to troponin, actomyosin dynamics and variable catalytic processes.

Acid-Base Equilibrium↗
PubMed1991

Whole-cell K+ currents in isolated rabbit corneal epithelial cells.

Membrane currents were recorded from enzymatically isolated cells from basal layers of rabbit corneal epithelium by the whole-cell clamp technique. Pipettes contained 140.4 mM KCl and extracellular K+ concentration was varied. The membrane currents on step voltage changes were rectangular currents with some fluctuations. The fluctuations disappeared near the zero-current potential. The reversal potential in normal Tyrode's solution with 5.4 mM K+ was -57.8 +/- 6.2 mV (mean +/- S.D., n = 10). Increasing [K+]o from 5.4 to 140.4 mM shifted the reversal potentials in the positive direction with a slope of 41.0 mV/decade. Concomitant depolarization of the resting potential was observed on increasing [K+]o. The whole-cell currents were blocked by Cs+ or Ba2+. These suggest that the major current component in the corneal epithelial cells in K+.

Animals↗
PubMed1990

Modulation of slow gating process of calcium channels by isoprenaline in guinea-pig ventricular cells.

1. The mechanism of enhancement of Ca2+ current by isoprenaline was studied by recording single-channel activity from cell-attached patches on isolated guinea-pig ventricular cells using patch pipettes containing 50 or 100 mM-Ba2+. 2. Isoprenaline (100 nM) increased the amplitude of ensemble average currents by increasing the rate of non-blank sweeps (availability). The current decay during 400 ms steps was significantly slowed by isoprenaline. However, the open probability for the non-blank sweeps elicited by 100 ms steps was only slightly increased by the application of isoprenaline. 3. The durations of the available state (TS) and the unavailable state (TF) were estimated by the number of non-blank and blank sweeps per run, respectively, applying repetitively 100 ms steps at 2 Hz. 4. At large negative holding potentials the distribution of TS was well fitted by an exponential curve, whose time constant was increased from 1.6 to 3.1 sweeps by 100 nM-isoprenaline, while TF distributed approximately single exponentially with a time constant of 2.0 sweeps in control and 1.3 sweeps in the presence of the drug. 5. At depolarized holding potentials a slow voltage-dependent component appeared in the histogram of TF and its time constant was markedly decreased by 100 nM-isoprenaline. 6. The availability-voltage relationship was simulated by the Boltzmann equation with a maximal value of 0.4 in the control. The maximal value was increased to 0.7 and the curve was shifted to a depolarizing direction by 7 mV by 100 nM-isoprenaline. 7. Isoprenaline increased the availability of cardiac Ca2+ channels by increasing the forward rate constant and decreasing the backward rate constant in both voltage-dependent and independent slow state transitions.

Animals↗
PubMed1990

Mechanism of adenosine-induced inhibition of calcium current in guinea pig ventricular cells.

The mechanism of adenosine-induced inhibition of Ca2+ currents was studied by recording single-channel Ca2+ currents from cell-attached patches on isolated guinea pig ventricular cells with pipettes containing 50 or 100 mM Ba2+. Numerous 100-msec depolarization steps were applied repetitively at 2 Hz from the resting potential of approximately -70 mV. The addition of 0.1 mM adenosine to the superfusate in the presence of 100 nM isoproterenol depressed the isoproterenol-induced increase in ensemble-averaged current: in peak amplitude, from 258 +/- 105% (mean +/- SD) (p less than 0.01) that of control in the presence of isoproterenol to 153 +/- 41% (n = 7) (p less than 0.05) by the addition of adenosine. In these patches, adenosine did not much affect the open probability in nonblank sweeps (control, 0.10 +/- 0.05; isoproterenol, 0.11 +/- 0.08; adenosine and isoproterenol, 0.08 +/- 0.05), but significantly decreased channel availability, defined as the rate of current-containing sweeps in total sweeps (control, 0.36 +/- 0.17; isoproterenol, 0.69 +/- 0.16 [p less than 0.01]; adenosine and isoproterenol, 0.45 +/- 0.20 [p less than 0.01]). The decrease of channel availability by adenosine was due to the shortening of the duration of the available state and the prolongation of that of the unavailable state. The depressive action of adenosine was suppressed by 0.1 mM theophylline. The single-channel conductance in the presence of 100 mM Ba2+ and Bay K 8644 was 26 pS and was not affected by isoproterenol or adenosine. We conclude that adenosine decreases Ca2+ current under beta-adrenergic stimulation mainly by reducing channel availability.

Adenosine↗
PubMed1989

[Experimental study of periodontal tissue regeneration using biodegradable membranes].

This study was designed to investigate the effect on new attachment formation using a biodegradable membrane as a barrier to the regeneration of periodontal tissue. One-wall wide periodontal osseous defects with exposed root surfaces were prepared in three adult mongrel dogs. After surgical debridement of the periodontal defects, 3 types of biodegradable membranes, [Poly(L-lactic acid); (P-L-LA)] membrane, [Poly(lactic acid-co-glycolic acid); (PLGA)] (81: 19 mole%) membrane and PLGA (50: 50 mole%) membrane, were arranged to cover the denuded root surfaces. Specimen blocks were removed 8 weeks postoperatively for histological evaluation of their effect on the regeneration of periodontal tissue. The results were as follows: 1. Gingival regions containing P-L-LA or PLGA (81: 19 mole%) membranes showed delayed wound healing macroscopically. 2. Almost all P-L-LA membranes were present in the experimental sites failing to be resorbed during the 8-week experimental period. PLGA (81: 19 mole%) membranes were also present but showed with some degree of resorption and fragility, while PLGA (50: 50 mole%) membranes were completely resorbed. 3. This showed that the membranes used in this experiment are possible barriers to the generation of new attachment. It is important to make sure keeping the membrane. 4. There was no relationship between osteogenesis and cementogenesis. It seems that osteogenesis was depressed by membrane shrinkage and the gingival pressure which limited "the regenerative space of bone." 5. Moderate resorption was observed on the root surface, and new cementum was formed at the resorbed surface. 6. Ankylosis was observed between the new cementum and bone at the experimental sites. Newly formed cementum was seen on coronal sections of this area.

Animals↗
PubMed1988

Voltage-dependent decrease in the availability of single calcium channels by nitrendipine in guinea-pig ventricular cells.

1. The mechanism of Ca2+ channel block by nitrendipine was studied by recording single-channel activity from cell-attached patches on guinea-pig ventricular cells using patch pipettes containing 50 mM-Ba2+. Test depolarization pulses to around 10 mV with a duration of 100 ms were applied repetitively at 2 Hz. 2. The percentage of non-blank sweeps was maximal (about 40%) at a holding potential between -65 and -130 mV and decreased sigmoidally with its depolarization. Nitrendipine shifted the availability-voltage relationship in a hyperpolarizing direction. 3. From the number of consecutive non-blank sweeps and that of blank sweeps, the duration of the available state and that of the unavailable state were estimated. 4. The histogram of the duration of the available state showed a single-exponential distribution. Its mean duration was about 1.5 s and was shortened by nitrendipine. Correspondingly, the decay of the mean current during the depolarization step was accelerated by nitrendipine. 5. In the presence of 100 nM-nitrendipine the histogram of the duration of the unavailable state at large negative holding potentials was simulated as the sum of two exponential components, one with a time constant similar to that in the control and the other with a time constant of 6-7 s. 6. The histogram of the duration of the unavailable state at depolarized holding potentials was simulated by a double-exponential curve also in the control. The duration of the slow component was prolonged by nitrendipine. 7. The prolongation of the unavailable states initiated by drug binding during depolarization steps and maintained during depolarized holding potentials is the mechanism of the blockade. The rate constants of the state transitions between an available state and two unavailable states were estimated.

Action Potentials↗
PubMed1987

Maitotoxin-activated single calcium channels in guinea-pig cardiac cells.

1. In order to clarify the mechanism of Ca-dependent excitatory action of maitotoxin (MTX), the most potent marine toxin known, patch-clamp techniques were used to analyse electrophysiological effects of MTX on guinea-pig isolated cardiac myocytes. 2. The whole-cell recordings showed that MTX (0.3 ng ml-1) produced a sustained inward current that was enhanced by adrenaline (2 microM) and abolished by Cd2+ (1 mM). 3. This current was predominantly carried by Ca2+ or Ba2+ and has an almost linear current-voltage relationship. 4. In cell-attached patches, MTX added to the pipette solution activated Ca channels with novel properties. The opening events of these channels occurred as long bursts, and the channel gating showed little voltage-dependence. 5. The unitary conductance was 12 pS in the presence of 50 mM Ba2+. Within a burst, the distribution of opening times was a single exponential with a mean open time of 10.4 ms. 6. The channel described here represents either a new class of voltage-independent Ca channel or an entirely modified form of voltage-gated Ca channel. This channel may account for the mechanism of enhanced Ca2+ influx through the cell membrane induced by MTX, and presumably regulates some ionic movements in myocardial cells.

Animals↗
PubMed1986

Beta-adrenergic modulation of the slow gating process of cardiac calcium channels.

Single Ca channel currents were recorded from isolated guinea pig ventricular myocytes in the presence of 50 mM Ba by the patch clamp technique under cell-attached configuration. When a constant short depolarizing pulse was applied repetitively, a single Ca channel opened in bursts during some depolarizing steps but completely failed to open in other steps. The opening probability of Ca channels in current-containing sweeps was little affected by adrenaline. There was a tendency for either failure, or success, in inducing a burst, to occur in clusters. The histogram of the number of successes between two failures showed a single exponential distribution with a time constant of 1-2 sec in controls and 2-4 sec in the presence of adrenaline (2 X 10(-6) M). The mean number of failures between two successes was diminished considerably by adrenaline. In ventricular myocytes adrenaline seems to increase the Ca current mainly by decreasing the rate of the Ca channel for the transition between one mode at which the channel is allowed to open on depolarization and other modes.

Adrenergic beta-Agonists↗
PubMed1978

The effect of procaine on the passive electrical properties of guinea-pig ventricular muscle.

Electrotonic potentials produced by rectangular hyperpolarizing current pulses were recorded intracellularly at various distances from guinea-pig papillary muscles and the results were analyzed according to the single-dimensional cable model. In normal Tyrode solution the space constant (lambda) was 0.62 +/- 0.12 mm (mean and S.D., nine preparations) and the time constant (tau) was 4.0 +/- 0.8 ms. Procaine (1 mg/ml) increased lambda to 1.20 +/- 0.29 mm and tau to 19.7 +/- 4.7 ms by increasing the membrane resistance, while the membrane capacity was only slightly increased and little change was observed in the internal longitudinal resistance. The dose-response relationship revealed that procaine inhibited the resting membrane conductance almost completely in a one-to-one manner with the dissociation constant of about 1 mM. It was suggested that potassium conductance predominant in the resting membrane conductance in guinea-pig papillary muscle was depressed by procaine and that electrical coupling is well maintained even when the membrane resistivity of apposed normal ordinary membrane at intercalated disks becomes high.

Animals↗
PubMed1976

Manganese-dependent propagated action potentials and their depression by electrical stimulation in guinea-pig myocardium perfused by sodium-free media.

1. Propagated action potentials were recorded in right ventricular papillary muscles from guinea-pig heart while exposed to Na-free, Ca-free and Mg-free solutions containing Mn. 2. When Na was totally replaced by 95 mM-Mn the overshoot was about 45 mV while the resting potential was about -90mV. 3. The overshoot of action potentials was increased by about 20-30 mV per tenfold increase of Mn concentration over the range of 2-50 mM. 4. Similar increases of overshoots with increasing of Mn concentration also occurred in the presence of 0-6 mM-Ca. Increasing of Ca from 5 to 20 mM had little influence on the overshoot but shortened the duration of the Mn-dependent action potential in the presence of 5 mM-MN. 5 Mn-dependent action potentials were not depressed by 3 X 10(5) M tetrodotoxin but by La. 6. These results suggest that Mn passes through the slow inward current channel to generate the action potential seen under the Na-free condition. 7. The overshoot and duration of the Mn-dependent action potential decreased with stimulation. At stimulus frequencies (Hz) of 0-5, 0-2, 0-1, 0-017 and 0-0033 the overshoot of action potential in 5 mM-Mn Tyrode decreased by 0-5-1 mV per an action potential. This depression of the action potential is explained by assuming intracellular accumulation of Mn.

Action Potentials↗
PubMed1975

Manganese action potentials in mammalian cardiac muscle.

The membrane potential in guinea-pig's papillary muscles from right ventricle was recorded by glass microelectrodes and stimulation was effected by current pulses applied through a sucrose-gap. Action potentials with overshoot were recorded in the solution lacking Na+ and Ca++ but containing 2-95 mM Mn++. The overshoot was increased with the increase of [Mn++]o by about 30 mV/decade. Similar Mn++ dependent action potentials were also obtained in Na-free solution containing 0.6 mM Ca++. The results indicate that Mn inward current is sufficient to generate action potentials in cardiac muscle.

Action Potentials↗