Negative surface charges provoke conformational change of membrane proteins and release of calcium from sarcoplasmic reticulum.
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Animals↗
Biomedical subjects
T Oba
Publications and source records attributed to T Oba.
[MR imaging of traumatic cerebellar dysfunction].
Four cases of cerebellar dysfunction following head trauma are presented. Cerebellar signs revealed were those such as dysmetria, dysdiadochokinesis, horizontal nystagmus and ataxia. T2-weighted magnetic resonance (MR) imaging (0.15 tesla, spin-echo method; TR 2000 msec. and TE 100 msec.) revealed focal lesions in these patients, although CT scan failed to demonstrate any changes in the cerebellum. The cerebellar symptoms were maximal immediately after the trauma but improved gradually in two cases. These are compatible with the transient traumatic cerebellar dysfunction postulated by R. C. Cantu in 1969. The pathophysiology of this syndrome, whether it is due to cerebellar concussion or contusion, has not yet been determined. The abnormality of the cerebellum revealed by MR imaging seemed to be contusion rather than concussion. Therefore the authors presume that transient traumatic cerebellar dysfunction is caused by minor cerebellar contusion. In the other two cases, delayed epidural hemorrhage ensued and the symptoms disappeared rapidly after evacuation of the hematoma. In these patients, occurrence of delayed epidural hematoma in the posterior cranial fossa was predicted by MR imaging. The authors regard the lesion as an alarm signal indicating the probable occurrence of infratentorial hematoma.
Adult↗
Calcium release from frog sarcoplasmic reticulum by an imidazolyl reagent.
Calcium is released from the isolated heavy sarcoplasmic reticulum (SR) of frog skeletal muscle upon application of 0.1-1 mM diethylpyrocarbonate (DEP, an imidazolyl reagent). The Ca-ATPase activity of SR was suppressed by 20% in the presence of 1 mM DEP. More than 1 mM of free magnesium ion or 5 microM ruthenium red eliminated the effect of DEP on calcium release but not on Ca-ATPase activity. A plausible site of DEP action is on the calcium channel.
Animals↗
Caffeine treatment inhibits drug-induced calcium release from sarcoplasmic reticulum and caffeine contracture but not tetanus in frog skeletal muscle.
Effects of pretreatment with caffeine on Ca2+ release induced by caffeine, thymol, quercetin, or p-chloromercuriphenylsulfonic acid (pCMPS) from the heavy fraction of sarcoplasmic reticulum (SR) were studied and compared with those effects on caffeine contracture and tetanus tension in single fibers of frog skeletal muscle. Caffeine (1-5 mM) did induce transient Ca2+ release from SR vesicles, but subsequent further addition of caffeine (10 mM, final concentration) induced little Ca2+ release. Ca2+ release induced by thymol, quercetin, or pCMPS was also inhibited by pretreatment with caffeine. In single muscle fibers, pretreatment with caffeine (1-5 mM) partially reduced the contracture induced by 10 mM caffeine. However, tetanus tension was almost maximally induced by electrical stimulus in caffeine-treated fibers. These results indicate that SR, which becomes less sensitive to caffeine, thymol, quercetin, or pCMPS by pretreatment with caffeine, can still respond to a physiological signal transmitted from transverse tubules.
4-Chloromercuribenzenesulfonate↗
Ruthenium red and magnesium ion partially inhibit silver ion-induced release of calcium from sarcoplasmic reticulum of frog skeletal muscles.
Effects of Ca2+-induced Ca2+ release blockers, ruthenium red (RR) and Mg2+, on Ag+-induced Ca2+ release were studied using skinned muscle fibers or fragmented heavy SR (HSR) prepared from frog muscle, and compared with those on caffeine-induced one. Exposure of the skinned fibers to 5 microM Ag+ produced a rapid and large contraction in the presence of 0.043 mM free Mg2+. When Mg2+ concentration was increased to 0.86 mM, Ag+ led to a large transient contraction, combined with a small tonic one. The transient component was completely blocked by high Mg2+ (3.64 mM), but the tonic one was not. Ca2+-ATPase activity was not stimulated by increase of Mg2+ from 0.86 to 3.64 mM. Ag+ and caffeine induced a rapid Ca2+ efflux from HSR in a dose-dependent manner. RR over a range from 1 to 10 microM dose-dependently inhibited the Ca2+ efflux induced by 10 microM Ag+. Despite increase of RR to 30 microM, however, further inhibition of the Ca2+ efflux was not produced any more (77.8 +/- 12.2% inhibition). A 10 mM caffeine-induced efflux of Ca2+ was blocked slightly by only 0.5 microM RR and almost completely by 3 microM. A slight inhibition (about 28%) of the Ca2+-ATPase activity was observed in the presence of 10 microM Ag+ in 0.5 mg SR protein/ml of medium. RR and caffeine did not affect the enzyme activity. These results indicate that frog SR could induce a rapid release of Ca2+ upon Ag+ and caffeine, suggesting that Ag+ may have two different binding sites to release Ca2+; one is on Ca2+-induced Ca2+ release channel and the other on RR-insensitive site.
Animals↗
Change in surface charge of sarcoplasmic reticulum membrane may elicit conformational change in sulfhydryl groups of membrane proteins to release calcium.
A lipophilic anion, tetraphenylboron (TPB-)-induced Ca2+ release from fragmented sarcoplasmic reticulum (SR) of frog skeletal muscle was monitored by chlortetracycline fluorescence. TPB- caused change in surface charge of the membrane and in the protein conformation with a time course similar to that of the Ca2+ release. Tetraphenylarsonium (TPA+) inhibited these effects of TPB-. Change in surface charge of SR is suggested to cause conformational change in SR membrane proteins, and then result in Ca2+ release from the SR.
Animals↗
Similar inhibitory effects of dantrolene sodium on twitch tension and on silver ion-induced contracture in skeletal muscle.
To determine the mechanism by which Ag+ induces a transient contracture in skeletal muscle, the effect of dantrolene sodium on the Ag+ contracture was examined and the findings compared with those for the twitch, tetanus and caffeine contracture. The inhibition of twitch by dantrolene was equivalent to that of the Ag+ contracture at concentrations of 1, 2 or 5 microM of dantrolene. The tetanus tension was slightly inhibited by dantrolene, but not the caffeine contracture. These observations suggest that the Ag+ contracture may be governed by the same mechanism as that involved in the development of twitch tension.
Animals↗
Effects of extracellular calcium and calcium channel blocker on silver-induced contractures in frog skeletal muscle fibers.
The mechanism by which Ag+ induces muscle contracture was elucidated by investigating the effect of external Ca2+ concentration and Ca2+ channel blocker on the maximum tension amplitude in single fibers from frog toe skeletal muscle. Five microM Ag+ induced two different types of contracture in the presence of external Ca2+ more than 0.1 mM, i.e., a phasic and a subsequent tonic contracture. The phasic contracture appeared only in fibers with intact T-tubules immersed in a solution with or without Ca2+ after a lag time of 5.7 +/- 0.9 s (N = 5). The maximum amplitude was 58% of the tetanus tension observed in the same fiber immediately before Ag+ exposure. Diltiazem at high-concentration (100 microM) inhibited the Ag+-induced phasic contracture only to a small extent (17%). The contracture was not affected by 1 microM TTX or 1 mM DAP at all. These results indicate that Na+, K+, and Ca2+ channels on the T-tubular membrane would not be attributed to the phasic tension development induced by Ag+. On the contrary, a tonic contracture did not require intact T-tubules. The amplitude and the rate of rise of the contracture depended on external Ca2+ concentrations and were inhibited by a high concentration of diltiazem. Neither 1 microM TTX nor 1 mM DAP affected them. Therefore, the tonic contracture seems to be triggered by Ca2+ which entered the muscle fiber through the surface but not T-tubular membranes.
4-Aminopyridine↗
A local anesthetic, tetracaine, similarly inhibits Ag+ and K+ contractures in frog skeletal muscle.
To evaluate usefulness of Ag+ contracture as a tool for elucidating the mechanism underlying the excitation-contraction coupling, the effects of tetracaine on Ag+ contracture were compared with those on K+ and caffeine contractures in frog skeletal muscle. Tetracaine less than 100 microM shortened the duration of 120 mM K+ contracture, without affecting tension amplitude. At higher concentrations of tetracaine, K+ contracture was inhibited dose-dependently and the duration shortened. Treatment of the fibers with 20-500 microM tetracaine for 3 min did not block the contracture induced by 25 mM caffeine. Effects of tetracaine on Ag+ contracture were similar to those on K+ contracture. In the presence of 200 microM tetracaine, 41% inhibition was observed in 120 mM K+ contracture, while 43% in 100 microM Ag+ contracture. Also, 200 microM tetracaine completely inhibited the contractures induced by 40 mM K+ or 5 microM Ag+. These findings suggest that the Ag+ may induce contractures via its action on the T/SR junction, not a direct action on the SR. Therefore, understanding the mechanism involved in the development of Ag+ contracture would be helpful to elucidate the mechanism of excitation-contraction coupling.
Action Potentials↗
Inhibition of Zn2+-induced potentiation of twitch tension by Ni2+ in frog muscle.
Effect of Ni2+ on Zn2+-induced potentiation of twitch tension was studied electrophysiologically in the toe muscle fibers of Rana catesbeiana. The major findings of this investigation are as follows. When 2 mM Ni2+ was applied to fibers in a normal Ringer's solution containing 50 microM Zn2+ (Zn2+ solution), the Zn2+-potentiated twitch tension decreased remarkably to about one-third of that before Ni2+ treatment. This concentration of Ni2+ caused a 23% decrease in the duration of action potential which had been prolonged by Zn2+ (6.61-5.09 ms). Ni2+ (2 mM) added to normal Ringer's solution led to increases of about 30 and 42% in twitch tension and in the duration of action potential, respectively. A slight increase in the mechanical threshold was induced by 2 mM Ni2+. The inhibitory action of Ni2+ on the twitch tension in Zn2+ solution was larger than that in the case of tetanus tension. Diltiazem (40 microM), a Ca2+ channel blocker, did not inhibit the twitch tension potentiated in Zn2+ solution. These results suggest that the decrease in Zn2+-potentiated twitch tension by Ni2+ may possibly derive from impairment of the propagation of action potential along the T tubules.
Action Potentials↗
Chemical modification of calcium release from the sarcoplasmic reticulum of mechanically skinned skeletal bullfrog muscle fibers.
Several types of reagents that react with amino acid side chains induced repetitive phasic contracture of skinned skeletal muscle from frogs. The presence of 10 mM procaine or 5 mM magnesium in the medium or disruption of the sarcoplasmic reticulum (SR) eliminated this contracture, indicating that the calcium-induced calcium-release mechanism of SR is involved in the contraction. Dithiothreitol inhibited the contracture induced by chloramine T, N-acetylimidazole, or p-chloromercuriphenylsulfonic acid (pCMPS) but not in the case of carbodiimide, phenylglyoxal, trinitrobenzenesulfonic acid, diethylpyrocarbonate (DEP), or N-chlorosuccinimide (NCS). Therefore, modification of groups other than the sulfhydryl ones seems to induce contractures under such conditions. The amplitude of the caffeine-induced contracture decreased after treatment with pCMPS, DEP, or NCS. NCS shifted the pCa-tension curve toward low pCa in the SR-disrupted fibers. This shift would explain the decrease in the caffeine contracture. It is tentatively concluded that pCMPS and DEP release a large amount of calcium from SR.
Animals↗
Silver ion-induced tension development and membrane depolarization in frog skeletal muscle fibres.
Silver ions elicit dose-dependently a transient contracture in single fibres of bull-frog toe muscle placed in 0-Ca2+, Cl- -free MOPS solution containing 3 mM Mg2+ and NO3-. To elucidate the mechanisms involved, changes in membrane potential and in tension development were continuously measured following exposure to Ag+. The effect of Ag+ on contraction in fibres in which the membrane had been depolarized by elevating the external K+ concentration was also examined. The major findings of this investigation are as follows. (1) The mechanical threshold was shifted towards more negative potentials by 5 mV (-51 to -56 mV), when Ca2+ and Cl- in the Ringer's solution were replaced with Mg2+ and NO3-, respectively. (2) On the exposure of the fibres to 5 microM Ag+, the membrane potential decreased by 1.6 mV from -87.8 mV and tension was developed. (3) In fibres soaked in a solution containing 10 mM K+ (corresponding to a membrane potential of -69.5 mV), 5 microM Ag+ produced a large contracture similar to that seen in the control solution. (4) The Ag+-induced contracture was inactivated when more than 20 mM K+ was used. (5) The membrane depolarization evoked by either 20 or 50 microM Hg2+ did not produce contraction. (6) Muscle fibres which had been exposed to 20 microM Hg2+ for 5 min responded to 5 microM Ag+ by a transient tension development. These findings strongly suggest that Ag+-induced tension development is not associated with depolarization of the surface membrane but rather is caused by specific actions of Ag+ on membrane proteins in the T-tubules.
Animals↗
Hg2+-induced contracture in mechanically skinned fibers of frog skeletal muscle.
In mechanically skinned fibers of the semitendinosus muscle of bullfrogs, we examined the role of membrane sulfhydryl groups on Ca2+ release from the sarcoplasmic reticulum (SR). Hg2+, a sulfhydryl reagent (20-100 microM), induced a repetitive contracture of skinned fibers, and this contracture did not occur in skinned fibers in which the SR had been disrupted by treatment with a detergent (Brij 58). Procaine (10 mM), Mg2+ (5 mM), or dithiothreitol (1 mM) blocked the Hg2+-induced contracture. Ag+ or p-chloromercuribenzenesulfonic acid produced similar contractures to that induced by Hg2+. We conclude that Hg2+ releases Ca2+ from SR of a skinned fiber by modifying sulfhydryl groups on the SR membrane, and suggest that the Ca2+ released by Hg2+ may trigger a greater release of Ca2+ from SR to develop tension.
Animals↗
Transient intracellular calcium movement coupled with mechanical activity of smooth muscle.
Change of intracellular free Ca in smooth muscle was monitored using Quin 2, Ca sensitive fluorescence dye. Upon electrical stimulus, increase of light emission from the sample occurred in two phases. Procaine and caffeine inhibited and facilitated, respectively, the 2nd phase of intensity change, which coincided with the mechanical response. It is concluded that the released Ca from intracellular store sites may play a key role for the mechanical activation of smooth muscles.
Aminoquinolines↗
Tension development in frog skeletal muscle induced by silver ions.
In single fibers of frog toe muscles placed in a Cl- free MOPS solution containing 1.8 mM Ca2+, tension developed slowly in the presence of very low concentrations of Ag+. This tension was not blocked by the administration of Co2+ or Ni2+. On the other hand, two types of transient tensions developed with the application of 5 microM Ag+, in fibers pretreated with 0-Ca2+ MOPS solution, containing either 2 mM Co2+ or 1mM Ni2+, for 10 min. In the presence of divalent cations or TTX, the first repetitive twitch-like contraction disappeared, indicating this tension is induced by action potentials repeatedly generated by the lack of divalent cations. The 2nd subsequent transient tension was caused by 5 microM Ag+ in the presence of various kinds of divalent cations, or TTX. After reversion to the resting tension, the fiber was contracted by adding more than 0.1 mM of Ca2+ or 25 mM caffeine to the external medium. Even when placed in a Ca2+-free solution containing 3 mM EGTA and 3 mM Mg2+ for 30 min, the fiber still developed an appreciable tension in response to 5 microM Ag+. These findings suggest that a transient development of the Ag+-induced tension does not require the presence of external Ca2+. A specific sulfhydryl reagent, pCMPS, did not contract the muscle fiber. Therefore, Ag+ may develop tension by mediating unknown chemical reaction(s) other than the sulfhydryl group on T-tubular membrane proteins.
4-Chloromercuribenzenesulfonate↗
[Analysis of apprehension of patients with repeated hospitalization concerning therapy and daily activities following discharge: a follow-up survey after discharge].
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Activities of Daily Living↗
Migration of acetylated hemicellulose from capillary hemodialyzer to blood, causing scleritis and/or iritis.
From November 1981 to early March 1982, an outbreak of scleritis and/or iritis occurred among patients treated with a Nipro brand NAC series cellulose acetate capillary dialyzer. The rate of incidence with dialyzers produced in 1982 was significantly higher than that with dialyzers produced in 1981. An extract obtained from the dialyzers caused iritis in rabbits after its infusion into an auricula vein. Glycerol, acetylated carbohydrate (AC) derivatives, urethane derivatives, and polypropyleneglycol were found in the extract. AC derivatives caused iritis in rabbits, whereas they caused hyperemia of the bulbar conjunctiva in dogs. The AC derivatives contained xylose and glucose units in a ratio of 1.6-2.3:1. The amounts of AC derivatives were significantly larger in the extracts from 1982 than from 1981 devices. Moreover, another brand, but the same type, of dialyzer, the Cordis Dow 4000, contained a slight amount of them. These facts show that AC derivatives derived from hemicellulose played a primary role in the outbreak.
Acetylation↗
Effect of temperature and Zn2+ on isometric contractile properties and electrical phenomena of frog (Rana) and Xenopus skeletal muscle fibers.
Effects of temperature and Zn2+ on the isometric contractile properties of toe muscle fibers of Rana catesbeiana and Xenopus laevis were studied. The maximum twitch tension almost doubled when the temperature was lowered from 20 to 4 degrees C in Rana muscles but not in Xenopus muscles, although the duration of action potential in Xenopus muscle was increased slightly more than that seen in the Rana species. The maximum rate of rise of tension was greater in Xenopus muscle than in the Rana muscle, at 20 degrees C. The prolongation of the time-to-peak tension following exposure to low temperature (4 degrees C) was more pronounced in Rana than in Xenopus muscles. These results suggest that the speed of release and reuptake of Ca2+ by the sarcoplasmic reticulum (SR) differs in Rana and Xenopus muscles and that these factors may be related to differences in the SR and the T-tubular morphology. In Rana muscles, Zn2+ prolonged the falling phase of the action potential and potentiated the twitch tension. In Xenopus muscles, Zn2+ marginally prolonged the duration of action potential and the twitch tension was not markedly potentiated. These results indicate that Zn2+ potentiates the twitch by prolonging the action potential and that Rana muscles are more sensitive to the effects of Zn2+.
Action Potentials↗