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S Sunano

Publications and source records attributed to S Sunano.

At least 73 records · Page 4Linked to original sources
PubMed1987

Effects of sodium vanadate on smooth muscles of guinea-pig ureter and their relation to extracellular Ca.

The effects of sodium vanadate on electrical and mechanical activities of the guinea-pig ureter were studied. Sodium vanadate at concentrations higher than 10(-5) M induced elevations of basal tension and repetitive twitch-like contractions. The drug depolarized membrane only slightly but induced repetitive action potentials. Sodium vanadate potentiated phasic and tonic contractions of K-contracture. It also increased tension development of high amplitude in K-depolarized preparations. Thus, the change in the resting membrane potential does not seem to play the only role in the initiation of contractions, though sodium vanadate-induced twitch-like contractions were associated by repetitive action potentials. Sodium vanadate-induced twitch-like contractions were blocked by Ca removal or by verapamil, but elevated basal tension was depressed only slightly under these treatments. Sodium vanadate induced tension development in the absence of Ca both in polarized and K-depolarized preparations. These results suggest that sodium vanadate increased mechanical activities by enhancing Ca influx as well as releasing intracellular bound Ca and/or inhibiting Ca extrusion through cell membrane.

Animals↗
PubMed1986

Effects of sodium vanadate on various types of vascular smooth muscles.

Effects of sodium vanadate on various vascular smooth muscles of guinea pigs, rabbits, and Wistar Kyoto rats (WKY) were studied. Sodium vanadate of concentrations higher than 10(-5) M induced contractions in the aortae of all animals. The contractile effects varied among vascular smooth muscles, and mesenteric arteries showed no or only weak contractile response to the drug, while aortae showed higher contractile responses. In the portal veins, potentiation of spontaneous contractions was observed by the application of sodium vanadate. These responses were not blocked by treatments with adrenergic blocking agents or indomethacin, indicating the direct action of the drug on vascular smooth muscles. Treatment with 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) blocked completely the contractile effects of sodium vanadate, whereas it showed no effect on K-contractures. Partial depolarization of the membrane by elevations of K concentration potentiated sodium vanadate-induced contractions and minimized the variations of responses among preparations. In K-depolarized preparations, sodium vanadate often induced relaxation of preparations. The contractile effects of sodium vanadate were not blocked by treatment with ouabain, though ouabain also showed contractile actions in a number of preparations. It was suggested that vanadate acts directly on vascular smooth muscles and causes contractions without relation to the inhibition of Na,K-ATPase. It may cause contractions inhibiting Ca-ATPase of sarcoplasmic reticulum and/or of cell membrane, and cause relaxation by inhibiting ATPase of contractile proteins. The variations of the responses may be explained by differences of membrane permeability to vanadate.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1986

Comparison of contractile effects of sodium vanadate and ouabain in vascular smooth muscles of guinea-pigs and rats.

Ouabain and vanadate are known as potent inhibitors of Na, K-ATPase in various tissues including smooth muscles. Both agents showed contractile action on various smooth muscles in a similar fashion: stronger contractile action on the aortae of rats (WKY and stroke prone spontaneously hypertensive rats, SHRSP) and guinea-pigs, and weaker contractile actions on basilar and mesenteric arteries of the same animals. Time to peak tension, however, was far longer in ouabain-induced contraction. Phentolamine depressed ouabain-induced contractions, while vanadate-induced contractions were not affected. Elevation of K+ concentration to 20 or 30 mM potentiated vanadate-induced contraction markely, while it potentiated ouabain-induced contraction only slightly. DIDS blocked vanadate-induced contraction but showed no effect on ouabain-induced contraction. Removal of Ca abolished ouabain-induced contractions, while vanadate-induced contractions of reduced height could be observed in the absence of Ca. Verapamil depressed both ouabain- and vanadate-induced contractions of WKY and SHRSP aorte aut exhibited no effect on the guinea-pig aorta. Thus, although similarities of the action of ouabain and sodium vanadate were observed, the modes of the actions were revealed to be different in the two agents. Inhibition of Na, K-ATPase might be involved in the case of ouabain-induced contractions, and inhibition of Ca-ATPase of membranous systems might be involved in vanadate-induced contraction.

Animals↗
PubMed1985

Contraction independent of extracellular Ca by sodium vanadate in guinea-pig vas deferens.

The effects of Ca removal and Ca antagonists on sodium vanadate-induced contractions of the guinea-pig vas deferens were studied. Sodium vanadate-induced tension development could be observed even 120 minutes after the removal of Ca, whereas K-contracture disappeared within 20 minutes. Spontaneous contractions induced by sodium vanadate were abolished by the removal of Ca. Verapamil and nifedipine did not show any effect on sodium vanadate-induced contraction, contrastingly, they blocked spontaneous contractions initiated by sodium vanadate. The effects of sodium vanadate on Ca contracture of depolarized preparations were also studied. Though the drug potentiated phasic contraction, it did not potentiate tonic component of Ca contracture. It was demonstrated that sodium vanadate induced tension development independently of extracellular Ca, presumably by releasing intracellularly bound Ca.

Animals↗
PubMed1985

Effects of sodium vanadate on the smooth muscle of the guinea-pig vas deferens.

Effects of sodium vanadate on electrical and mechanical activities of smooth muscle of the guinea-pig vas deferens were investigated. Sodium vanadate of concentrations higher than 5 X 10(-6) M caused an elevation of basal tension and, at concentrations higher than 5 X 10(-4) M, initiated spontaneous contractions. These effects were not blocked by treatments with reserpine, tetrodotoxin or phentolamine. Treatment with ouabain also did not block the tension development by sodium vanadate. Sodium vanadate caused slight depolarization of membrane and potentiated spike activities. The phasic contraction of potassium contracture was potentiated by sodium vanadate in a similar manner to pretreatment with 15 mM K+ or with ouabain, both treatments occasioning slight depolarization. Sodium vanadate also caused tension development in K-depolarized preparetions. Contrastingly, drug-induced contractions were not significantly affected by sodium vanadate. It is suggested that sodium vanadate acts directly on smooth muscles and causes tension development without relation to Na, K-ATPase activity. Changes in the membrane electrical activities may be part of the cause of contraction. However, it can also initiate tension development without membrane potential changes, presumably acting on intracellular Ca binding sites.

Animals↗
PubMed1984

The effects of Ca antagonists, manganese and lanthanum on cooling-induced contracture of depolarized vas deferens.

Lowering of temperature applied during the course of the tonic contraction of high-K-induced contracture of guinea-pig vas deferens induced an increase in tension which was sensitive to extracellular Ca. Verapamil and nifedipine inhibited the tonic contraction and cooling-induced tension development. Mn2+ and La3+ also showed inhibiting actions on the tonic contraction, which, however, was followed by slow re-elevation of the tension. Cooling treatment caused relaxation in the presence of either ion, which increased with repetition of the cooling treatment. By rewarming the preparation, a phasic contraction, which increased in height with repetition of the treatment, was observed. These effects in the presence of Mn2+ or La3+ were also observed in the absence of Ca or in preparations treated with caffeine in Ca-free solution (Ca-deprived preparation). Verapamil was capable of depressing these effects of Mn2+ and La3+. These results suggest the involvement of influxed Ca in the initiation of tension development by cooling. The decrease of extrusion through the cell membrane and/or uptake by intracellular binding sites at low temperature may be the cause of the cooling-induced tension development. Mn2+ or La3+ induces the tension development by their direct actions on contractile proteins which are differently affected by the changes in temperature.

Animals↗
PubMed1984

Stimulating and potentiating effects of sodium nitroprusside on the guinea-pig vas deferens and their comparison with the effects on the portal vein and the taenia coli.

The effects of sodium nitroprusside on the electrical and mechanical properties of the guinea-pig vas deferens were studied and compared with those on the portal vein and the taenia coli. Sodium nitroprusside at concentrations higher than 0.5 mM caused depolarization of the membrane of the vas deferens and initiated spontaneous contractions, while spontaneous contractions of the portal vein were blocked by similar concentration of the drug. Noradrenaline- and carbachol-induced contractions of the vas deferens were markedly potentiated by sodium nitroprusside, whereas the noradrenaline-induced contraction of the portal vein was suppressed by the same concentration of the drug. Increasing the K+ concentration by 15 to 30 mM caused a similar potentiation of the contraction by noradrenaline or carbachol in the vas deferens. When sodium nitroprusside was applied during the course of noradrenaline- or carbachol-induced contracture, contraction was observed in the vas deferens, while relaxation was induced in the portal vein and taenia coli. In either case, however, the addition of Ca caused a relaxation of the preparations. These results suggest that the membrane depolarization may be involved in the stimulating effects sodium nitroprusside in the guinea-pig vas deferens.

Animals↗
PubMed1984

The effects of sodium nitroprusside on the phasic and tonic contraction of the potassium contracture of the smooth muscle of guinea-pig vas deferens and portal vein.

The effects of sodium nitroprusside on potassium-induced phasic and tonic contraction of the guinea pig vas deferens and portal vein were studied. Sodium nitroprusside at concentrations higher than 10(-4) M potentiated the phasic contraction of potassium contracture of the vas deferens, while it showed no or slight depressing effect on the tonic contraction. Sodium nitroprusside at the same concentration depressed both the phasic and tonic contractions of the portal vein. Sodium nitroprusside depolarized the membrane of the vas deferens but did not alter the depolarization by K-Tyrode's solution. Potentiation of the phasic contraction was also observed following the pretreatment with 20 mM K+. When sodium nitroprusside was applied during the course of the tonic contraction, marked relaxation was observed in the portal vein, while only slight relaxation was induced in the vas deferens even by high concentrations of the drug. Residual tension in the presence of sodium nitroprusside was completely abolished by the application of verapamil of the concentration higher than 10(-6) M. Relaxations of preparation by sodium nitroprusside were counteracted by increases in Ca concentration. When sodium nitroprusside was applied in the presence of moderately elevated-K+ (15 to 30 mM), an increase in tension was observed in the vas deferens and a decrease in tension was observed in the portal vein. The differences in the action of sodium nitroprusside on the vas deferens and on the portal vein may be explained by the differences in the action of the drug on cell membrane, especially on the membrane potential.

Animals↗
PubMed1982

The direct inhibitory action of phentolamine on the contraction of rabbit basilar artery.

The effects of phentolamine on rabbit basilar artery were studied and compared with those on other smooth muscles. The drug showed a dose-dependent depressing effect on high-potassium-induced contracture of rabbit basilar artery. The depressing effect was stronger on tonic than on phasic contraction. When phentolamine was applied during high-potassium-induced tonic contraction, dose-dependent relaxation was observed. The degree of phentolamine-induced-relaxation of high-potassium-induced tonic contraction was not affected by surgical denervation of the basilar artery, although catecholamine content was almost completely lost, as indicated by chemical and histochemical experiments. The relaxed tension caused by phentolamine was reversed by addition of Ca in a dose-dependent manner. Verapamil also showed a dose-dependent relaxing effect on high-potassium-induced contracture, with this relaxed tension being reversed by the addition of Ca in a dose-dependent manner. The relaxing effect of phentolamine on rabbit basilar artery was stronger than on rabbit aorta or guinea-pig taenia coli. Phentolamine depressed serotonin- or histamine-induced contraction at a concentration more than 10 times higher than the concentration for depression of noradrenaline-induced contraction. The depression of high-potassium-induced contracture and reversal by additional Ca, especially in denervated preparations, indicates that phentolamine acts directly on smooth muscle in a similar manner to that of Ca antagonists.

Animals↗
PubMed1982

[Actions of manganese and lanthanum on smooth muscles].

Effects of Mn2+ and La3+ on the excitation, contraction, ion movement, and biochemistry of smooth muscles were reviewed. Both Mn2+ and La3+ block the action potential of smooth muscles without affecting membrane resting potential. However, depolarization or hyperpolarization by these ions and slow discharges which are not affected by these ions have also been reported in some smooth muscles. Mn2+ and La3+ inhibit the spontaneous contraction and high-K-induced contracture, although these ions can also initiate slow tension development in some preparations. The drug-induced contractions are relatively insensitive to these ions. Mn2+ blocks Ca influx, and La3+ blocks both Ca influx and efflux. However, La-resistant Ca movements such as Na-Ca exchange or active Ca extrusion have also been reported. La3+ also shows effects on the movement of other ions. In biochemical experiments, La3+ shows effects on Ca movement of the membraneous and microsomal fractions of smooth muscles, with variations among the smooth muscles. Thus, we should be careful of using these ions as mere Ca blockers.

Acetylcholine↗
PubMed1981

Factors affecting high-potassium-induced contracture of guinea-pig vas deferens.

Some factors which may influence the high-K-induced contracture of guinea-pig vas deferens were studied. Portional variations were observed in the height of tonic contraction but not in phasic contraction; tonic contraction was higher on the epididymal side and lower on the prostatic side. Circular muscle showed contracture similar to that of longitudinal muscle in the shapes of the contracture and the tendency to portional variations. Histological variations of muscle structure could not explain these variations. Electrical stimulation of the preparation by continuous weak AC current induced contracture similar to the high-K-induced contracture. The contracture evoked by AC stimulation was blocked by TTX and phentolamine. Blocking agents of possible transmission involved in high-K depolarization did not alter the relation of phasic and tonic contractions, although some of the drugs showed an inhibiting and some an enhancing effect. In isotonic observations, tonic contraction was highly sensitive to load and was elevated with a low load and depressed with a high load. It was revealed that the phasic and tonic contraction of high-K-induced contracture was a direct reaction of longitudinal muscle, although various factors could have had some influence on the contracture.

Animals↗
PubMed1981

The initiation of phasic and tonic contraction by potassium and the effect of calcium, multivalent cations and Ca-antagonist on potassium contracture in guinea-pig vas deferens.

The role of Ca in phasic and tonic contractions of high-K-induced contractures of guinea-pig vas deferens was studied. It was shown that phasic contraction was initiated by a burst of action potentials, and tonic contraction by sustained depolarization. Phasic contraction seemed to be related to the rate and degree of depolarization, whereas tonic contraction seemed to be related only to the degree of depolarization. Tonic contraction was more sensitive to a reduction of extracellular Ca, though both types of contraction were abolished by Ca removal. The tonic contraction observed with isotonic recording was more sensitive to extracellular Ca than that observed with isometric recording. Maximum contractions were achieved with lower Ca than that in isometric measurement. Verapamil blocked tonic contraction at a low concentration, and both contractions at a high concentration. Mn or La blocked the phasic and tonic contractions first. After prolonged exposure to either ion, however, tonic contraction could be induced. The results suggest that both phasic and tonic contractions were induced by Ca-influx through the cell membrane, and that tonic contraction was maintained by a constantly elevated intracellular Ca concentration which is the consequence of an altered equilibration of Ca influx and Ca extrusion through the cell membrane.

Action Potentials↗
PubMed1981

A comparison of the effects of temperature and metabolic inhibition on the contraction of smooth muscle.

The effects of temperature and metabolic inhibitors on short tetanus contraction of vas deferens were studied. The contraction height increased by lowering temperature from 35 degrees C, and decreased with a decrease in temperature below 25 degrees C. The maximum speed of contraction and relaxation decreased by lowering the temperature, showing a transition of Q10 values at 25 degrees C. The Q10 value for the maximum speed of contraction was 1.7 between 35 to 25 degrees C, and 5.3 between 25 to 10 degrees C. The Q10 value for the maximum speed of relaxation was 1.9 between 35 and 25 degrees C, and 13.0 between 25 and 15 degrees C. The time to peak tension and to half relaxation increased by lowering temperature. The Q10 values also showed a transition at 25 degrees C. The Q10 value for the time to peak tension was -2.5 between 35 and 25 degrees C, and -5.0 between 25 to 5 degrees C. The Q10 value for the time to half maximum relaxation was -3.1 between 35 and 25 degrees C, and -5.7 between 25 and 5 degrees C. NaN3 and KCN and DNP inhibited the contraction. However, time to peak tension and half maximum relaxation time were not altered. Although the maximum speed of contraction and relaxation decreased, this was caused only by the reduction in peak tension. O2-free or glucose-free treatment caused only a slight decrease in peak tension. Neither time to peak tension nor half maximum relaxation time was altered. The differences between the effects of temperature and metabolic inhibition are discussed.

2,4-Dinitrophenol↗
PubMed1981

[Elevation of extracellular K and its potentiation of the response to vasoactive substances in the rabbit basilar artery (author's transl)].

The authors have suggested from an in vitro study that extracellular K concentration can be elevated up to 40 Mm, when hemolysis of a clot occurs after subarachnoid hemorrhage. The present experiments were performed to investigate the change in contractility of rabbit basilar artery to vasoactive substances in the presence of increased K. The conclusion was as follows. 1. The contraction heights induced by serotonin (5 x 10(-7) M) were increased 2.4 +/- .02 fold, 6.4 +/- 0.3 fold, 5.7 +/- 0.4 fold (n = 10), when the K concentration of physiological solution was elevated to 8.1 mM, 13.5 mM, 24.3 mM, respectively. 2. Similar potentiation was obtained in prostaglandin F2 alpha. The tensions induced by prostaglandin F2 alpha (2.5 x 10(-6) M) were increased 2.3 +/- 0.3 fold, 4.7 +/- 0.4 fold, 3.7 +/- 0.4 fold (n = 6), whereas the responses to norepinephrine were rather less potentiated and the maximum height was 2.2 +/- 0.2 fold (n = 8) in 13.5 mM K. 3. Enhancement of the responses to vasoactive agents was also observed in the presence of tetraethylammonium (TEA). These results indicated that slight depolarization of membrane would potentiate the contractile responses to various vasoactive substances and that an increase in sensitivity could be a possible cause of cerebral vasospasm.

Animals↗
PubMed1980

[Smooth muscle and cardiac glycosides (author's transl)].

Actions of cardiac glycosides (C.G.) on smooth muscles are reviewed. 1. C.G. inhibit the Na-K ATPase of smooth muscle membrane, though the degree and mode of the inhibition vary among the types of smooth muscles. 2. The uptake of C.G. by smooth muscles has been reported to be influenced by K+, Na, ATP, and temperature. The difference between the uptake and its effect can be observed. 3. Intracellular K concentration decreased and intracellular Na concentration increased by the treatment with C.G. 4. They depolarized the membrane; the action being affected by extracellular ion concentration. An increase in spike discharges is observed. 5. C.G. potentiate or inhibit the concentrations of smooth muscles, depending on the types of smooth muscles and the causes of the contraction. C.G. can also cause transient contraction of smooth muscle. 6. C.G. influence the Ca content and Ca movements of smooth muscles. 7. C.G. cause the release of noradrenaline, acetylcholine, or prostaglandins. These substances can affect the contractile responses of smooth muscles.

Animals↗