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H Kontani

Publications and source records attributed to H Kontani.

At least 37 records · Page 2Linked to original sources
PubMed1988

In vivo inhibitory effects of stimulation at the central end of the pelvic nerve severed from urinary bladder on urinary bladder contraction in rats.

Two- or five-Hz electrical stimulation of the central end of the left pelvic nerve severed from the urinary bladder in rats inhibited bladder contraction induced by intravesical infusion of Tyrode's solution. Inhibition of bladder motility by 2-Hz nerve stimulation appeared after pretreatment with strychnine (0.3 mg/kg, i.v.), naloxone (1 mg/kg, i.v.) and picrotoxin (1 mg/kg, i.v.). Hypogastric nerve stimulation, however, did not affect bladder contraction. These results suggest the presence of an inhibitory mechanism on the pelvic motoneuron activated by contralateral pelvic nerve stimulation in rats.

Animals↗
PubMed1988

The effect of baclofen on the urinary bladder contraction accompanying micturition in anesthetized rats.

We studied the effects of baclofen on the bladder contraction induced by infusion of Tyrode's solution into the urinary bladder in anesthetized rats. Baclofen (5 mg/kg, i.v.) completely inhibited bladder contraction and abolished the efferent discharges recorded from the left pelvic nerve, causing the bladder pressure to rise until solution leaked from the penis. The inhibitory effect of baclofen (5 mg/kg, i.v.) could not be reversed by picrotoxin (1 mg/kg, i.v., twice with an interval of 10 min) or naloxone (1 mg/kg, i.v.). In parallel with convulsion, strychnine (1 mg/kg, i.v.) contracted the bladder which had been inhibited by baclofen and generated electrical activities consisting of efferent discharges and electromyograms. The dose of intracerebroventricularly or intrathecally injected baclofen which completely inhibited the bladder contraction was 0.1 or 10 micrograms, respectively. After the inhibition of bladder contraction by i.v. injection of baclofen, electrical stimulation of the sacral cord could contract the bladder and cause a fall in bladder pressure to around the level existing after micturition. From these results, the active site of baclofen which is related to the inhibition of bladder contraction is thought to be the micturition center in the brain stem.

Aminooxyacetic Acid↗
PubMed1988

A study of morphine-induced urinary retention in anesthetized rats capable of micturition.

The nature of morphine-induced urinary retention was studied in anesthetized rats in which the bladder contraction accompanying micturition could be observed. Morphine (0.1 mg/kg, i.v.) prolonged the micturition interval and increased the level of micturition threshold. Morphine (1 mg/kg, i.v.) completely inhibited bladder contraction and bladder pressure was elevated until solution leaked from the penis, but the bladder pressure after inhibition by morphine (1 and 5 mg/kg, i.v.) did not significantly rise over the peak pressure level during micturition before injection of morphine. The inhibitory effect of morphine (1 and 5 mg/kg, i.v.) was reversed by naloxone (0.1 mg/kg, i.v.). Morphine (5 mg/kg, i.v.) did not increase the pressure induced by infusion of solution from near the bladder neck to the urethra. After intracerebroventricular (i.c.v.) and intrathecal (i.t.) administration of morphine (1 microgram), the micturition interval was prolonged and the level of micturition threshold was increased. Morphine (5 micrograms, i.c.v. and i.t.) inhibited bladder contraction and naloxone (5 micrograms, i.c.v. and i.t.) reversed the inhibitory effect of morphine injected by the same administration route. From these results, urinary retention induced by systematically injected morphine was considered to result from inhibition of bladder function mediated via opioid receptors of the micturition centers in the supraspinal and spinal regions.

Animals↗
PubMed1987

[Central muscle relaxant activities of 2-methyl-3-aminopropiophenone derivatives].

In this experiment, we synthetized new 2-methyl-3-aminopropiophenone (MP) derivatives, whose structure is known to have central muscle relaxant activities, and quinolizidine and indan . tetralin derivatives derived from MP by cyclization, and we investigated the central muscle relaxant activity. Among the quinolizidine derivatives, there was a very strong central depressant agent, trans (3H, 9aH)-3-(p-chloro) benzoyl-quinolizidine (HSR-740), and among the indan . tetralin derivatives, there was an excitant agents, trans (1H, 2H)-5-methoxy-3, 3-dimethyl-2-piperidinomethyl indan-1-ol (HSR-719). From the results, these derivatives were not considered to be adequate for central muscle relaxant. Among the MP derivatives, (4'-chloro-2'-methoxy-3-piperidino) propiophenone HCl (HSR-733) and (4'-ethyl-2-methyl-3-pyrrolidino) propiophenone HCl (HSR-770) strongly inhibited the cooperative movement in the rotating rod method using mice, and it exerted almost the same depressant activity on the cross extensor reflex using alpha-chloralose anesthetized rats. However, the inhibitory effects of HSR-733 on the anemic decerebrate rigidity and the rigidity induced by intracollicular decerebration in rats were weaker than those of HSR-770 and eperisone. In spinal cats, at a low dose (5 mg/kg, i.v.), HSR-733 depressed monosynaptic and dorsal root reflex potentials as compared with polysynaptic reflex potentials, and inhibitory effects of HSR-733 on these three reflex potentials were more potent than those of eperisone and HSR-770. Although HSR-770 acts on the spinal cord and supraspinal level on which eperisone has been reported to act, HSR-733 may mainly act on the spinal cord. These results indicate that the MP derivative with a 2-methyl group may be suitable as a central muscle relaxant. HSR-770, which has equipotent muscle relaxant activity to eperisone, exerted strong inhibitory effects on oxotremorine-induced tremor and weak inhibitory effects on spontaneous motor activity in the Animex method using mice, as compared with eperisone.

Animals↗
PubMed1987

In vivo effects of drugs that act on the autonomic nervous system on the rat urinary bladder contraction accompanying micturition.

We prepared an experimental system to study the effects of drugs on urinary bladder contraction and micturition simultaneously in rats anesthetized with urethane (1 g/kg, s.c.) and alpha-chloralose (25 mg/kg, s.c.). When Tyrode's solution was infused at a constant rate (0.8-1 ml/10 min) through a needle inserted into the bladder from the left ureter, the bladder pressure gradually and then steeply rose, and micturition took place. These changes in bladder pressure and micturition were constantly repeated. In this model, drugs which partially inhibited the bladder contractile force, e.g., atropine (0.01-1 mg/kg, i.v.) and hexamethonium (C6, 5 mg/kg, i.v.) increased the frequency of bladder contraction instead of decreasing the amount of solution excreted from the penis by bladder contraction. The rate of afferent discharges during bladder filling was increased after injection of atropine or C6, and this increase was considered to be responsible for the induction of the increase in the frequency of bladder contraction. Drugs which inhibited the bladder contraction and interrupted micturition, e.g., C6 (20 mg/kg, i.v.) raised the bladder pressure until the solution leaked from the penis. As phentolamine (5 mg/kg, i.v.) or propranolol (1 mg/kg, i.v.) did not facilitate bladder motility but rather inhibited it, the inhibitory action of sympathetic nerves on bladder motility was considered to be weak in rats. This model was useful for studying the effect of drugs on bladder motility and micturition reflex.

Animals↗
PubMed1987

In vivo effects of gamma-aminobutyric acid on the urinary bladder contraction accompanying micturition.

We studied the effects of the gamma-aminobutyric acid (GABA) receptor agonists, diazepam and muscimol, on the urinary bladder contraction induced by infusion of Tyrode's solution into the bladder in anesthetized rats. Diazepam (1 mg/kg, i.p.) completely inhibited bladder contraction, causing the bladder pressure to rise until solution leaked from the penis. The inhibitory effects of diazepam were reversed by picrotoxin (1 mg/kg, i.v., twice with an interval of 10 min), and the effects were potentiated and attenuated by pretreatment with aminooxyacetic acid (AA, 10 mg/kg, i.v.) and semicarbazide (200 mg/kg, i.v.), respectively. Only pretreatment with AA inhibited the bladder contraction induced by infusion of Tyrode's solution into the bladder in six out of eight rats. Diazepam abolished efferent discharges recorded from the left pelvic nerve, but hexamethonium facilitated the generation of efferent discharges after inhibition of bladder contraction. After complete inhibition of bladder contraction by diazepam, electrical stimulation of the left pelvic nerve at 5 Hz for 30 sec was able to induce bladder contraction, and this resulted in micturition. Intracerebroventricular injection or intrathecal injection into the sacral part of the spinal cord of 1 microgram muscimol completely inhibited the bladder contraction. It was considered that the inhibitory effects of GABA receptor agonists on bladder contraction were mainly induced through the GABA receptors in the micturition center of the sacral cord, as well as the brain stem.

Aminooxyacetic Acid↗
PubMed1987

Pharmacological studies of the new centrally acting muscle relaxant 4'-ethyl-2-methyl-3-pyrrolidinopropiophenone hydrochloride.

The pharmacological properties of 4'-ethyl-2-methyl-3-pyrrolidinopropiophenone hydrochloride (HSR-770), a new centrally acting muscle relaxant, were investigated in experimental animals. HSR-770, within a dose range of 1-10 mg/kg i.v., relaxed alpha- and gamma-rigidities in rats, the dose required to relax gamma-rigidity being lower than the dose required to relax alpha-rigidity. When HSR-770 was intraduodenally (i.d.) administered within a dose range of 25-50 mg/kg, the relaxant activity on alpha-rigidity was potent and long-lasting in comparison with eperisone or tolperisone. HSR-770 inhibited flexor reflex more strongly than patellar reflex in a dose-dependent manner within a dose range of 2.5-10 mg/kg i.v. or 25 and 50 mg/kg i.d. in anesthetized cats. In spinal cts, HSR-770 (5 and 10 mg/kg i.v.) inhibited flexor reflex but this potency was weaker than that in anesthetized cats. HSR-770 (12.5-50 mg/kg i.d.) inhibited he crossed extensor reflex in anesthetized rats. In spinal cats, HSR-770 inhibited mono- and polysynaptic reflex potentials to the same extent and also depressed dorsal root reflex potential at 5 and 10 mg/kg i.v. HSR-770 at a dose (50 mg/kg p.o.) which exerted muscle relaxant activity on both rigidity and flexor reflex, had little effect on spontaneous motor activity (mice), hexobarbital-induced sleeping time (mice) and conditioned avoidance response (rats). These results indicate that HSR-770 is a potent centrally acting muscle relaxant and that its central nervous system depressant activity is relatively weak.

Anemia↗
PubMed1985

The effects of tetrodotoxin, papaverine and verapamil on the increase in the rate of spontaneous afferent discharges induced by local anesthetics from the pulmonary mechanoreceptors of the bullfrog.

Procaine (1 X 10(-5)-1 X 10(-4) M), dibucaine (1 X 10(-5)-1 X 10(-4) M) and tetracaine (1 X 10(-6)-1 X 10(-5) M) caused an increase followed by a decrease in the rate of spontaneous afferent (A) discharges (D) accompanied with a decrease in the flow rate of perfusion solution from the pulmonary vein in the isolated lung of the bullfrog, but these local anesthetics only decreased the rate of A.D. synchronized with lung inflation. The stimulatory effects of these drugs on the rate of spontaneous A.D. were studied. In the presence of TTX (1 X 10(-7) M), the increase in the rate of spontaneous A.D. by local anesthetics was inhibited, but the decrease in the flow rate of perfusion solution by these drugs was not inhibited. Papaverine (1 X 10(-5) M), which inhibited the decrease in the flow rate of perfusion solution by these local anesthetics, inhibited the increase in the rate of spontaneous A.D. by dibucaine, but not those by procaine and tetracaine. The inhibitory effects on the increase in the rate of spontaneous A.D. by these local anesthetics could be seen with verapamil in a concentration (1 X 10(-4) M) which significantly inhibited the rate of spontaneous A.D., like TTX (1 X 10(-7) M). Verapamil could not reverse the decrease in the flow rate of perfusion solution by these local anesthetics. From these result, the increase in the rate of spontaneous A.D. by procaine and tetracaine is due to not only the contractile effects of the drugs on the pulmonary vessel but also the direct stimulatory effects on the receptors which generate spontaneous A.D., and the increase in the rate of spontaneous A.D. by dibucaine may result from the contraction of the pulmonary vessel, and the stimulatory effect of dibucaine on the receptors would be weaker than that of procaine and tetracaine, since dibucaine could cause the increase in the rate of spontaneous A.D. only when dibucaine decreased the flow rate of perfusion solution.

Aconitine↗
PubMed1985

The effects of morphine and morphine-related compounds on the rate of afferent discharges from the pulmonary receptors in bullfrog.

We examined the effects of morphine and morphine-related compounds on the rate of afferent discharges from the pulmonary receptors in bullfrog. Morphine (1 X 10(-5) - 1 X 10(-3) M) decreased the rate of spontaneous afferent discharges in a concentration-dependent manner, but hardly affected the rate of afferent discharges synchronized with lung inflation. Dihydrocodeine, naloxone and dextrorphan had the same effects as morphine. Levallophan (1 X 10(-4) M), pentazocine (1 X 10(-4) M) and pethidine (1 X 10(-3) M) clearly decreased both rates of the spontaneous afferent discharges and the afferent discharges synchronized with lung inflation. In the presence of naloxone or levallorphan at the concentration of 1 X 10(-5) M, morphine (1 X 10(-5) and 1 X 10(-4) M) caused an additive decrease in the rate of afferent discharges. Dextromethorphan and apomorphine at the concentration of 1 X 10(-4) M caused an increase in the rate of spontaneous afferent discharges followed by decrease in both rates of the spontaneous afferent discharges and the afferent discharges synchronized with lung inflation. When dextromethorphan or apomorphine was washed out and the rates of afferent discharges were almost restored to the levels before application of each drug, reapplication of these drugs caused no increase in the rate of spontaneous afferent discharges, but the drugs inhibited the generation of afferent discharges. All of these drugs did not affect the flow rate of perfusion solution from the pulmonary vein.

Animals↗
PubMed1983

Effects of local anesthetics, tetrodotoxin, aconitine and verapamil on the mechanoreceptors of isolated frog heart.

Effects of local anesthetics, tetrodotoxin (TTX), aconitine and verapamil on the rate of afferent discharges from the mechanoreceptors of isolated hearts of the bullfrog were studied. When procaine (1 X 10(-4) M), tetracaine (1 X 10(-6) M) and dibucaine (1 X 10(-5) M) decreased the contractile force and beating rate of the heart, high frequency discharges that were synchronized with the contraction of the heart appeared. When concentrations of these local anesthetics were increased, the afferent discharges were abolished. When TTX (1 X 10(-8) M - 1 X 10(-7) M) caused a cardiac arrest, high frequency discharges, consisting of maintained discharges and the discharges synchronized with small contractions of the ventricle, appeared. Occasionally, in the presence of TTX (1 X 10(-7) M) the cardiac arrest occurred, and then very irregular contractions appeared. At that time, high frequency discharges synchronized with contractions appeared. On the other hand, aconitine (1 X 10(-7) M - 1 X 10(-6) M) initially increased the rate of afferent discharges from mechanoreceptors in the atrium and ventricle and then abolished the discharges without significantly affecting beating rhythms and contractile force. When verapamil (1 X 10(-6) M - 1 X 10(-5) M) was applied, the beating rate and contractile force were significantly decreased, but high frequency discharges synchronized with contractions were observed. These results indicate that local anesthetics, TTX and verapamil at those concentrations which depressed the cardiac functions did not inhibit the heart mechanoreceptor excitability and the concentration of aconitine that markedly affected the cardiac functions stimulated the heart mechanoreceptor.

Aconitine↗
PubMed1982

Pharmacological studies on supersensitization. VII. Inhibitory effect of dibenamine on cocaine-induced supersensitivity of isolated vas deferens of guinea pig.

Effects of dibenamine on cocaine-induced supersensitivity of isolated vas deferens of guinea pig were examined. Dibenamine at 1.0 x 10(-7)-1.0 x 10(-5) M attenuated the degree of cocaine-induced increase in sensitivity to acetylcholine without any effect on acetylcholine-contraction. The degree of dibenamine-induced inhibition was dependent on the concentration of dibenamine and inversely related to the concentration of cocaine. Dibenamine at the concentration capable of inhibiting the contractile response to norepinephrine did not affect the degree of the increase in sensitivity to norepinephrine induced by cocaine. Dibenamine diminished the degree of cocaine-induced increase in sensitivity to potassium in standard Tyrode solution and that in maximum response to calcium in partially depolarized vas deferens. Dibenamine at the concentration of 3.2 x 10(-7) M did not affect acetylcholine-contractions and attenuated potassium-contractions of the preparations exposed 5 min to calcium-free Tyrode solution, but the degree of cocaine-induced potentiation of contractile response in calcium-free Tyrode solution was not affected by dibenamine. These results suggest that cocaine-induced increase in calcium influx from extracellular fluid is selectively inhibited by dibenamine.

Acetylcholine↗
PubMed1981

Recording of pulmonary afferent activities from receptors in the perfused lung preparation of bullfrog and effects of drugs on the afferent activities.

Afferent activities from receptors in the isolated lung of the bullfrog were recorded. Volley of afferent discharges synchronized with inflation of the lung and spontaneous discharges in the resting expiratory position were observed. When the solution of pH 9.5 was perfused in the pulmonary circulation, the rate of afferent discharges was slightly increased. When the pH was decreased to 5.5, the perfusion rate decreased and the rate of discharges was slightly increased initially, then markedly decreased. The amount of perfusion solution from the pulmonary vein per min and the firing frequency were almost restored to pretreatment level after the lung was perfused with normal Ringer's solution. When the temperature of the solution was from 20 degrees C to 10 degrees C, the rate of discharges was decreased. Epinephrine (1 x 10(-4) M) and 4-aminopyridine (1 x 10(-4) M and 1 x 10(-3) M) produced an increase in the rate of discharges in proportion to decrease in the perfusion rate. Histamine (1 x 10(-4) M) did not influence the firing frequency and the amount of perfusion solution from the vein per min. This method enables recording of the effect of drugs on the pulmonary afferent activities.

4-Aminopyridine↗
PubMed1981

[Action of divalent cations on the mechanoreceptor of isolated frog heart (author's transl)].

Afferent activities were recorded in vagosympathetic nerves from mechanoreceptors of the isolated heart of bullfrog. The rate of discharges was increased when Ca2+ or Mg2+ (1.1 approximately 4.4 mM) was added to normal Ringer's solution containing 1.1 mM Ca2+. In terms of increase in the rate of discharges following the addition of Ca2+, an increase in the tone of cardiac muscle at diastole was observed. The rate of discharges was decreased and thereafter abolished within 5 to 10 min by lowering Ringer's solution Ca2+ concentration from 1.1 to 0.37 mM. A high firing frequency was observed with the addition of Mg2+ (0.73 mM) in the low Ca2+ Ringer's solution containing 0.37 mM Ca2+ and the rate remained unchanged for at least 15 min. On the other hand, the discharges were reduced, concentration dependently, when Mn2+ (0.22 approximately 1.1 mM) was added to normal Ringer's solution. When Mn2+ (0.22 or 0.55 mM) was applied, the rate of discharges decreased gradually and the reduction of discharges decreased 10 to 20 min after application. It appears that increase in the rate of discharges by application of Ca2+ is mainly the result of an increase in the tone of cardiac muscle induced by Ca2+. The presence of Ca2+ in external medium seems to be necessary to maintain the generation afferent discharges and Mg2+ can act as a substitute for Ca2+ in the generation of afferent discharges. The inhibitory effect of Mn2+ seems to be the result of depression of mechanoreceptors but the receptor becomes insensitive to Mn2+ within 10 to 20 min during exposure to low concentrations of Mn2+.

Action Potentials↗
PubMed1976

[Effect of drugs affecting sodium permeability on the muscle spindle of frogs].

Afferent discharges of about 10 Hz were recorded in the nerve from the isolated muscle spindle of the m. extensor longus digiti IV of the bullfrog subjected to a sustained stretch. When grayanotoxin-I, ventridine or aconitine was added to the Ringer's solution, the rate of discharges markedly increased and thereafter decreased. In these terms of decrease of discharges, abortive spikes were observed. The rate of discharges was markedly decreased by the application of procaine, diphenylhydantoin, chlorpromazine or tetrodotoxin. With the latter three drugs, abortive spikes were observed in the course of decrease of discharges. Increase of the discharge rate induced by grayanotoxin-I, veratridine and aconitine was antagonized by procain. No alteration was evident in the conduction of afferent discharges, when test drugs were applied to the nerve trunk in concentrations sufficient to change the rate of discharges when applied to the muscle spindle. These results suggest that the rate of the muscle spindle discharges is closely related to sodium permeability of the membrane.

Aconitine↗