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Biomedical subjects

H Kontani

Publications and source records attributed to H Kontani.

At least 19 recordsLinked to original sources
PubMed2005

Universality in heavy fermion systems with general degeneracy.

We discuss the relation between the T2 coefficient of electrical resistivity A and the T-linear specific-heat coefficient gamma for heavy-fermion systems with general N, where N is the degeneracy of quasiparticles. A set of experimental data reveals that the Kadowaki-Woods relation, A/gamma2=1 x 10(-5) muOmega cm(K mol/mJ)2, collapses remarkably for large-N systems, although this relation has been regarded to be commonly applicable to the Fermi liquids. Instead, based on the Fermi-liquid theory we propose a new relation, A /gamma2=1 x 10(-5) with A =A/1/2N(N-1) and gamma =gamma/1/2N(N-1). This new relation exhibits an excellent agreement with the data for the whole range of degenerate heavy fermions.

Journal Article↗
PubMed2000

Effects of adrenergic alpha2-receptor agonists on urinary bladder contraction in conscious rats.

We investigated the effects of the adrenergic alpha2-receptor agonists clonidine, oxymetazoline and tizanidine on bladder contractions induced by infusing fluid into the bladders of conscious male rats. I.v. clonidine and oxymetazoline (both 0.01 to 0.1 mg/kg) caused bladder hyperactivity, expressed by shortening of the intercontraction interval. Tizanidine (0.1 mg/kg, i.v.) caused slight shortening of the intercontraction interval. The rank order of potency was clonidine = oxymetazoline >> tizanidine. Intrathecal (i.t.) injection of 10 microg clonidine and oxymetazoline, and intracerebroventricular (i.c.v) injection at 15 microg, produced almost the same pattern of bladder hyperactivity as that observed after i.v. injection of these drugs (0.03 mg/kg, i.v.). For all three administration routes of clonidine and oxymetazoline, i.v. idazoxan (0.3 mg/kg) exerted an inhibitory effect on the bladder hyperactivity induced by these drugs, except i.c.v injection of oxymetazoline. I.t. phenylephrine (30 microg) did not change the intercontraction interval. Although i.c.v. phenylephrine (15 microg) shortened the intercontraction interval, the potency was weaker than those of i.c.v. clonidine and oxymetazoline (15 microg). These results suggest that clonidine and oxymetazoline cause bladder hyperactivity by acting at adrenergic alpha2 receptors in the micturition centers of the lumbosacral and supraspinal regions.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2000

Sex differences in urethral pressure response to electrical stimulation of the hypogastric nerves in rats.

PURPOSE: This experiment was performed to study the pharmacology of transmitters mediating the response, and the characteristics of the hypogastric nerve (HGN) of female rats, because electrical stimulation of the HGN was found to unexpectedly reduce urethral pressure in female rats. MATERIALS AND METHODS: Male and female Wistar rats (weighing about 250 gm.), 10 weeks and 6 months old, respectively, were used under anesthesia. Fluid was infused from the bladder neck into the urethral lumen at a constant rate (0.5 ml./10 minutes), and infusion pressure signals were measured. Bilateral HGNs were electrically stimulated at 5 and 10 Hz for 30 s. RESULTS: Electrical stimulation of the HGN reduced urethral infusion pressure in about 80% of the female rats, and the introduction of N(omega)-nitro-L-arginine methylester (L-NAME, 30 mg./rat, i.v.) elevated the urethral pressure response from a reduced state. Prazosin (0.1 mg./kg., i.v.) and hexamethonium (10 mg./kg., i.v.), which inhibited elevation of urethral pressure in male rats, also reversed and inhibited the elevation of urethral pressure in the female rats treated with L-NAME. CONCLUSION: The HGN in female rats contained nerve endings that released nitric oxide (NO) and norepinephrine (NE). NO released during HGN stimulation inhibited the release of (NE) and reduced urethral infusion pressure in female rats. Nerves with synapses in the pelvic ganglia released NE in both male and female rats, but nerves that released NO did not have synapses in the ganglia. Only NE was released from the HGN nerve endings in male rats.

Adrenergic Agents↗
PubMed1999

Inhibitory effects of tetrandrine and related synthetic compounds on angiogenesis in streptozotocin-diabetic rodents.

Structure-activity relationships of tetrandrine, isolated from a Kampo medicine, Stephania tetrandrae S. MOORE (root), and related synthetic compounds, were investigated in in vitro fetal bovine serum (FBS)-stimulated angiogenesis of cultured choroids in streptozotocin-diabetic Wistar rats, and air-pouch granuloma angiogenesis in vivo in diabetic mice. Tetrandrine, KS-1-1 (6,7-dimethoxy-1-[[4-[5-(6,7-dimethoxy-2-methyl-1,2,3,4-tetrahydroiso quinolinyl)methyl-2-methoxy]phenoxy]benzyl]-2-methyl-1,2,3,4-tetrahyd roisoquinoline), and KS-1-4 (6,7-dimethoxy-1-[[4-[4-(6,7-dimethoxy-2-methyl-1,2,3,4-tetrahydroiso quinolinyl)methyl]phenoxy]benzyl]-2-methyl-1,2,3,4-tetrahydroisoquino line), potently inhibited choroidal angiogenesis and air-pouch granuloma angiogenesis in the diabetic state. Their inhibitory effects on diabetic choroids were greater than those on normal choroids. Among these compounds, KS-1-4 inhibited only diabetic angiogenesis. These compounds significantly inhibited FBS-stimulated tube formation in vascular endothelial cells from normal rats. Tetrandrine and KS-1-4, but not KS-1-1, inhibited vascular endothelial growth factor- and platelet-derived growth factor-BB-stimulated angiogenesis in normal choroids. The bis[tetrahydroisoquinoline] moiety, connected by oxy-bis[phenylenemethylene] and 2,2'-dimethyl groups in tetrandrine, contributes to the inhibition of diabetic choroidal angiogenesis. KS-1-4 may be a candidate for anti-choroidopathy and retinopathy drugs in the diabetic state.

Alkaloids↗
PubMed1999

Effect of K+ channel openers, KRN2391 and Ki1769, and nitroglycerin on the urinary tract of rats in vivo.

The effects of KRN2391 (N-cyano-N'-(nitroxyethyl)-3-pyridine carboximidamide methane-sulfonate), which possesses ATP-sensitive potassium (K+) channel opening (KCO) activity and nitrate activity; Ki1769 (N-cyano-N'-(phenylethyl)-3-pyridinecarboximidamide methanesulfonate), which possesses only KCO activity; and nitroglycerin (NG) were determined on the motility of the ureter, urinary bladder and urethra of rats. Bladder contraction was induced by infusion of fluid into the bladder of conscious rats and recorded on a cystometrogram. KRN2391 and Ki1769 (both 0.3 mg/kg, i.v.) prolonged the micturition interval immediately after the injection, but NG (5 mg/kg, i.v.) did not. Peristaltic movement of the ureter, recorded in anesthetized rats, was inhibited by i.v. injection of KRN2391 and Ki1769 (both 0.03 mg/kg). However, when NG, NaNO2, N-nitro L-arginine methylester and methylene blue were applied directly to the ureter, no change in movement of the ureter was detected. KRN2391 (0.03 mg/kg, i.v.) and Ki1769 (0.3 mg/kg, i.v.) reduced the resistance to fluid infusion through the urethral lumen in anesthetized rats, whereas NG (0.5 mg/kg, i.v.) only reduced this resistance transiently. These results indicate that KCO activity had an inhibitory effect on the motility of the ureter, bladder and urethra. On the other hand, nitrate activity had an inhibitory effect on urethral tonus, corresponding to that induced by KCO activity.

Animals↗
PubMed1999

Effects of nifedipine on bladder overactivity in rats with cerebral infarction.

PURPOSE: Our objective was to evaluate the effect of the calcium (Ca2+) channel blocking agent nifedipine on bladder overactivity induced by middle cerebral artery (MCA) occlusion and determine its site of action. MATERIALS AND METHODS: Seven days after implantation of a bladder catheter, a cannula for intracerebroventricular and intrathecal administration was implanted and the left MCA was occluded with 4-0 monofilament nylon thread in male SD rats. Twenty-four hours after the induction of cerebral ischemia, saline was infused into the bladder at a constant rate (200 microL/min.) and cystometrogram was measured in conscious state. Nifedipine was administered intracerebroventricularly (5 microL) or intrathecally (20 microL) at graded doses (0.15 ng.-0.15 microg., 0.15 microg. -1.5 microg., respectively). RESULTS: Bladder capacity in conscious rats was significantly reduced after the left MCA occlusion. Intracerebroventricular administration of nifedipine significantly increased bladder capacity in cerebral infarcted rats but not in sham operated rats. Furthermore there was no significant difference in bladder capacity between before and after intrathecal administration of nifedipine in cerebral infarcted rats. CONCLUSION: These results show that Ca2+ channel blocking agents can operate especially on the supraspinal central nervous system rather than on the spinal system in rats with neurogenic bladder overactivity following cerebral infarction.

Animals↗
PubMed1998

A quantitative assay for angiogenesis of cultured choroidal tissues in streptozotocin-diabetic Wistar and spontaneously diabetic GK rats.

Angiogenesis of cultured choroids was quantitatively assayed in spontaneously diabetic GK and a bolus-treated streptozotocin (STZ)-diabetic Wistar rats. The number and total length of microvessels budded from cultured choroidal explants were measured to use as angiogenic indices. Both indices in 10-week-old Wistar rats were increased in parallel by 5% fetal bovine serum (FBS) from days 2 to 7 in culture. These indices in STZ-rats (10 weeks of age) were increased by 5% FBS to a greater extent than those in age-matched normal rats. These enhanced actions of FBS were concentration-dependent. The explants of 16-week-old GK rats also increased these indices to a greater extent than those of age-matched Wistar rats. Aging to 18 weeks of age also increased choroidal angiogenesis in the normal rats. In conclusion, the assay model of choroidal angiogenesis was established by determining the number and length of microvessels in cultured choroidal explants. The diabetic states of STZ-Wistar and GK rats enhanced FBS-induced choroidal angiogenesis. This assay model is useful for determining angiogenic activity of growth factors and effective drugs in diabetic choroidopathy and retinopathy.

Aging↗
PubMed1997

Urinary bladder response to hypogastric nerve stimulation after bilateral resection of the pelvic nerve or spinal cord injury in rats.

BACKGROUND: We examined the mechanism of urinary bladder motility return after bladder areflexia induced by interruption of the sacral parasympathetic outflow to the urinary bladder following damage to the sacral cord or pelvic nerves in the rat. METHODS: The L6 and S1 nerve bundles were resected near the vertebrae, and bilateral pelvic nerve resections (PNR) performed. Spinal cord injury (SCI) was performed by means of a legion generator at the T12 vertebra. Thirty days after PNR and SCI, cystometrograms were recorded under anesthesia. RESULTS: In all rats subjected to PNR or SCI, overflow incontinence continued, yet some rats subjected to SCI recovered within 2 weeks after the operation. Cystometrograms showed that repetitive bladder contractions appeared in rats subjected to SCI irrespective of hypogastric nerve (HGN) innervation, while bladder contractions did not appear in rats subjected to PNR. Electrical stimulation of the HGN induced higher bladder pressure elevation in rats who underwent PNR than in rats subjected to SCI. CONCLUSIONS: These results suggest that the generation of repetitive bladder contractions induced by bladder distention after bladder areflexia requires the presence of intact pelvic nerves that transmit sacral cord-originating excitatory information to the bladder. However, the HGN system and functioning pelvic nerve ganglia are not involved in this process. Also, the connection from the preganglionic HGN to the postganglionic parasympathetic nerves in the pelvic plexus did not form after PNR.

Animals↗
PubMed1993

A simple method for measurement of ureteric peristaltic function in vivo and the effects of drugs acting on ion channels applied from the ureter lumen in anesthetized rats.

In supine anesthetized rats, two cannulae were inserted into a unilateral ureter near the kidney and urinary bladder, respectively. Fluid from a reservoir placed approximately 27 cm above the rat was infused into the ureter lumen through the cannula near the kidney, and the resulting peristaltic pressure signals were measured from the cannula near the bladder. When drugs acting on ion channels were applied from the ureter lumen and their effects on the peristaltic pressure signals were studied, the K+ channel opener BRL 38227 (1 x 10(-4) M and 1 x 10(-3) M) was found to decrease the frequency dose-dependently. However, the K+ channel blockers glibenclamide and 4-aminopyridine at 1 x 10(-3) M did not affect peristaltic movement. Nifedipine (1 x 10(-5) M and 1 x 10(-4) M) decreased the frequency of peristalsis, but the effect was weaker than that of BRL 38227. Lidocaine at very high concentration (1.5 x 10(-2) and 1.5 x 10(-1) M) decreased the amplitude and increased the frequency of the peristaltic signals. These results indicate that the K+ channel opener has the most inhibitory effect on ureteral peristaltic function.

4-Aminopyridine↗
PubMed1993

Effects of levcromakalim on ureteral peristaltic function and cystometrogram in rats.

We studied the effect of levcromakalim on the function of the urinary tract in rats. Using anesthetized rats, ureteral peristaltic movement of only the ureter region or the ureter with the kidney was induced by fluid infusion into the ureter lumen. Levcromakalim (0.03 and 0.3 mg/kg, i.v.) exerted a stronger inhibitory effect on the peristaltic movement of the ureter region distant from the pelvis than on that near the pelvis, and the inhibitory effect of levcromakalim (0.03 mg/kg, i.v.) was not antagonized by glibenclamide (0.1 mg/kg, i.v. or 10 mg/kg, i.p.). Topical application of levcromakalim (injection volume, 0.1 ml; 10(-4) or 10(-3) M), which was injected via a vessel near the ureter inhibited ureteral peristaltic movement and the inhibitory effect levcromakalim (10(-4) M), was not antagonized by glibenclamide (10(-3) M) injected via the same route. Levcromakalim (0.3 mg/kg, i.v.) did not interrupt micturition in anesthetized and conscious rats. In conscious rats, the micturition interval was prolonged; and in anesthetized rats, the peak pressure during micturition was reduced. After injection of levcromakalim (0.3 mg/kg, i.v.), vesicoureteral reflux did not occur. In the movements of the ureter, urinary bladder and urethra, levcromakalim exerted the strongest inhibitory effect on the ureteral peristalsis.

Administration, Topical↗
PubMed1992

Effects of adrenergic agonists on an experimental urinary incontinence model in anesthetized rabbits.

We have developed an experimental urinary incontinence model in anesthetized female rabbits, in order to study the effects of alpha-adrenergic receptor agonists on it in vivo. Micturition was induced artificially by electrical stimulation of the abdomen of rabbits receiving a continuous infusion of glucose-free. Tyrode's solution into the urinary bladder. Alpha-1 adrenergic agonists, phenylephrine (1 mg/kg, i.v.) and the newly synthesized agent ST-1059 (1 mg/kg, i.v.) and its prodrug midodrine (10 mg/kg), which was intraduodenally administered, elevated the bladder pressure and arrested micturition induced by electrical stimulation. Prazosin (0.1 mg/kg, i.v.) inhibited these effects of phenylephrine. The effect of an alpha-2 agonist, clonidine (1 mg/kg, i.v.), on micturition induced by electrical stimulation was not clearly defined. This study demonstrates that alpha-1 adrenergic agonists can arrest artificially-induced micturition via urethral contraction. This method may be useful for evaluating the effect of a drug on urethral leakage in vivo.

Adrenergic alpha-Agonists↗
PubMed1992

Involvement of alpha 2-adrenoceptors in the sacral micturition reflex in rats.

We have studied the effects of intrathecally-injected drugs that act on alpha-adrenoceptors in the urinary bladder reflex contractile activity evoked by continuous infusion of fluid into the bladder of anesthetized rats. Clonidine (10 and 30 micrograms) facilitated and yohimbine (100 micrograms) abolished the bladder contractile activity, and pretreatment with yohimbine (30 micrograms) inhibited the effect of clonidine (10 micrograms). Phenylephrine (60 micrograms) abolished the bladder contractile activity, but prazosin (40 micrograms) had no significant effect on it. The bladder contractions induced by electrical stimulation of the pontine micturition center were inhibited by yohimbine in a dose-dependent manner. These results suggest that transmission in the descending neurons from the pontine micturition center to the sacral parasympathetic neurons that control bladder motility is mediated by alpha 2-adrenoceptors in rats.

Animals↗
PubMed1990

Effects of apomorphine on urinary bladder motility in anesthetized rats.

We studied the effects of apomorphine (AM) on bladder motility in anesthetized rats in which Tyrode's solution was continuously infused into the bladder at a constant rate, including an almost constant rate of bladder contraction accompanying micturition. AM at a dose of 1 mg/kg, i.v., caused a hyperactive bladder response, during which micturition disappeared. AM (12.5 micrograms for intracerebroventricular (i.c.v.) injection or 50 micrograms for intrathecal (i.t.) injection also caused a hyperactive response in about half of the rats. Supersensitization to AM appeared in reserpine-treated rats (2.5 mg/kg, i.p., 48 and 24 hr before the experiment). Haloperidol (1 mg/kg, i.v.) or SCH 23390 (5 mg/kg, i.v.) completely suppressed the hyperactive bladder response induced by AM (5 mg/kg, i.v.), and then the bladder contraction accompanying micturition reappeared after administration of these drugs. Pretreatment with sulpiride (100 mg/kg, i.p.) for 60 min, which hardly affected the bladder contraction induced by infusion of Tyrode's solution, suppressed the hyperactive bladder response induced by AM. These results suggest that the hyperactive bladder response induced by i.v.-injected AM results from synchronous stimulation of the micturition reflex centers in the brain stem and sacral cord and that the hyperactive bladder response is elicited via both D1 and D2 receptors.

Anesthesia↗
PubMed1990

Evaluation of drugs for treatment of urinary bladder dysfunction in conscious rats with intact pelvic nerve and after resection of the left pelvic nerve.

We studied the effects of drugs used for treatment of bladder dysfunction in conscious rats with intact pelvic nerves and also in rats at one or two weeks after nerve decentralization on the left side. Bladder contraction accompanying micturition was continuously induced by infusion of solution at a constant rate. When the effects of oxybutynin (3 mg/kg, i.p.) and terodiline (3 and 10 mg/kg, i.p.) on the cystometrogram were studied for about 2 hr, these drugs shortened and then prolonged the micturition interval (MI), but atropine (1 and 5 mg/kg, i.p.), butylscopolamine (20 mg/kg, i.p.) and nifedipine (3 mg/kg, i.p.) exhibited only a shortening effect on the MI. After injection of oxybutynin (10 mg/kg, i.p.), solution dribbled from the urethra for about 30 min. Terodiline (3 mg/kg) caused ischuria in the rats one week after resection of the left pelvic nerve, but not in the rats two weeks after surgery. Physostigmine (0.3 mg/kg, i.p.) improved micturition in the rats one week after surgery, but the effect was not evident in the rats with intact pelvic nerves. It was found that the drugs used for treating failure to store or expel urine exhibited a beneficial effect on micturition in rats with intact pelvic nerves and also in rats one week after nerve decentralization, respectively.

Animals↗
PubMed1990

Dopamine receptor subtypes that induce hyperactive urinary bladder response in anesthetized rats.

In anesthetized rats, SKF 38393 (10 mg/kg, i.v.) did not facilitate urinary bladder motility, but bromocriptine (BR, 5 mg/kg, i.v.) alone and the combination of BR (1 mg/kg, i.v.) and SKF 38393 (1 mg/kg, i.v.) induced a hyperactive bladder response (HBR). Both HBR induced by BR alone or BR and SKF 38393 combined was suppressed by SCH 23390, sulpiride or haloperidol. These results indicate that HBR is mediated by the activation of D-2 receptors, and the effects of D-2 agonists on bladder motility are potentiated by the simultaneous stimulation of D-1 receptors.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1989

Effects of central nervous system-acting drugs on urinary bladder contraction in unanesthetized rats.

We studied the effects of drugs on urinary bladder contraction in unanesthetized (UA) rats using the same method as that previously employed to investigate similar effects in urethane and alpha-chloralose-anesthetized (A) rats. The surgical procedure was performed under halothane anesthesia, and after the recovery, the rats were restricted in a Ballman cage during the experiment. The pattern of the cystometrogram obtained in UA rats was very similar to that in A rats, and almost the same pattern was maintained for at least three hours. Baclofen (10 mg/kg, i.p.), morphine (10 mg/kg, i.p.) and pentobarbital (20 mg/kg, i.p.) completely inhibited the bladder contraction at doses only double those at which the same drugs inhibited the bladder contraction in A rats when i.v. injected. When the bladder pressure rose almost to the level of the peak pressure existing before injection of these drugs, the instilled solution leaked from the penis. On the other hand, even after injection of diazepam (5 mg/kg, i.p.) at a dose five times greater than the minimum amount necessary for complete inhibition of bladder contraction in A rats, the bladder contraction accompanying micturition continued in UA rats. It appears that the inhibitory effect of diazepam on bladder contraction in rats is potentiated by anesthesia.

Anesthesia↗