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Biomedical subjects

Y Kasuya

Publications and source records attributed to Y Kasuya.

At least 199 records · Page 11Linked to original sources
PubMed1992

Involvement of serotonergic mechanisms in the inhibitory effect of U-50,488H on glutamate-induced lethality in mice.

The present study showed the involvement of serotonergic mechanisms in the protective effect of U-50,488H, a selective agonist of kappa-opioid receptors, against glutamate-induced lethality in mice. U-50,488H (1-10 mg/kg, i.p.) protected mice to a significant extent against glutamate-induced lethality, in a dose-related manner. This protective effect was not observed in p-chlorophenylalanine- or methysergide-treated mice. These results suggested that 5-HT in the brain may play an important role in the protective effect of U-50,488H against glutamate-induced lethality.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1992

Abnormalities of the autonomic nervous system of the duodenum in streptozotocin-induced diabetic rats.

The changes in sensitivity of the rat duodenum to ATP were examined in preparations from control rats and from rats with streptozotocin (STZ)-induced diabetes. ATP was able to relax the duodenum of control animals in a concentration-dependent manner and this relaxation was significantly increased in STZ-diabetic rats. In preparations from diabetic rats, relaxation responses to ATP were greater than those of age-matched control groups. These results suggest that functional changes or degeneration of non-adrenergic, non-cholinergic nerves in the myenteric plexus may occur in STZ-diabetic rats, and that these alterations may result in the increased sensitivity of the relaxation of the duodenum to ATP.

Adenosine Triphosphate↗
PubMed1992

Serotonin release in nucleus of the solitary tract and its modulation by antitussive drugs.

The effects of antitussive drugs on the release of [3H]5-hydroxytryptamine ([3H]5-HT) were investigated in slices prepared from rat nucleus of the solitary tract (NTS) and depolarized with 30 mM KCl under superfusion conditions. Dihydrocodeine and dextromethorphan, both central acting antitussive drugs, significantly increased the release of [3H]5-HT from slices of the rat NTS. Furthermore, these antitussive drugs significantly increased the rate of turnover of the 5-HT in the brainstem. These results suggest that the effect of central acting antitussive drugs were mediated by increase of 5-HT release in the brainstem, particularly in the NTS.

Animals↗
PubMed1991

Effects of 8-hydroxy-2-(di-n-propylamino)tetralin, a selective agonist of 5-HT1A receptors, on the cough reflex in rats.

The effects of the agonist of 5-HT1A receptors, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), on the capsaicin-induced cough reflex in rats were studied. I.p. injection of 8-OH-DPAT, at doses of 0.1 and 0.3 mg/kg, significantly decreased the number of coughs in a dose-dependent manner. The antitussive effect of 8-OH-DPAT (0.3 mg/kg) was blocked by prior injection of methysergide (3 mg/kg i.p.) and spiperone (0.3 mg/kg i.p.), whereas ketanserin (3 mg/kg i.p.) had no effect on the antitussive effect of 8-OH-DPAT. The antitussive effects of dihydrocodeine (1 mg/kg i.p.) and dextromethorphan (3 mg/kg i.p.) were also antagonized by methysergide and spiperone. However, these cough-depressant effects were not reduced by ketanserin. These results suggest that the antitussive action of 8-OH-DPAT may be related to the enhancement of the function of 5-HT1A receptors, and that antitussives interact with the 5-HT1A receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1991

Modulation of mu-mediated antitussive activity in rats by a delta agonist.

Effects of selective mu and delta receptor agonists on capsaicin-induced cough reflex in rats were studied. Intracisternal injection (i.cist.) of a selective mu receptor agonist [D-Ala2,Mephe4,Gly-ol5]enkephalin (DAMGO) produced dose-related depression of coughs over the 0.003-0.03 nmol dose range. The antitussive potency of DAMGO was 100-fold more potent than morphine. The antitussive effects of DAMGO and morphine were significantly reduced by naloxone (1 nmol i.cist.). The selective delta receptor agonist, [D-Pen2,D-Pen5]enkephalin (DPDPE), at a dose of 10 nmol (i.cist.), had no significant effect on the number of coughs. When co-administered i.cist., DPDPE (10 nmol) consistently and significantly decreased the antitussive potencies of DAMGO and morphine. The decrease in the antitussive effects of DAMGO and morphine caused by DPDPE were prevented by selective delta receptor antagonist, naltrindole (3 nmol). These results suggest that the antitussive effects of opioids are mediated predominantly by mu receptors, and delta receptors may play an inhibitory role in antitussive processes that are mediated by the mu receptors.

Aerosols↗
PubMed1991

Potassium channel opening properties of a novel compound, NIP-121, cromakalim and nicorandil in rat aorta and portal vein.

A novel compound, NIP-121, cromakalim and nicorandil caused concentration-dependent relaxation of rat aortas precontracted with 30 mM KCl, with pEC50 (M) values of 8.2, 7.1 and 5.5, respectively. At 60 mM KCl, the vasorelaxation induced by NIP-121 or cromakalim was almost abolished whereas that induced by nicorandil remained. In preparations precontracted with prostaglandin F2 alpha(PGF2 alpha) (10(-5) M), glibenclamide (10(-7) M) and phentolamine (3 x 10(-6), 3 x 10(-5) M) antagonized the relaxation induced by NIP-121 and cromakalim but not that induced by nicorandil. Methylene blue (10(-5) M) showed antagonistic effects against the vasorelaxation induced by nicorandil but not that induced by NIP-121. NIP-121 (10(-7), 10(-6) M) and cromakalim (10(-6), 10(-5) M) significantly increased the 86Rb+ efflux rate in rat aorta. The three compounds inhibited the frequency of spontaneous contractions of the rat portal vein (pIC30; NIP-121 = 8.0, cromakalim = 7.1 and nicorandil = 4.9); glibenclamide and phentolamine antagonized the effects of these compounds. In conclusion, NIP-121 is a more potent K+ channel opener than cromakalim in these tissues. Nicorandil apparently behaves as a K+ channel opener in the rat portal vein, but the vasorelaxation may involve some other mechanisms, such as generation of cyclic GMP.

Animals↗
PubMed1991

Phosphoramidon inhibits the intracellular conversion of big endothelin-1 to endothelin-1 in cultured endothelial cells.

Effects of various protease inhibitors on the conversion of big endothelin (ET)-1 to ET-1 in cultured endothelial cells were analyzed. A metal protease inhibitor, phosphoramidon, decreases the amount of ET-1 and increase that of big ET-1 released. This effect is dose-dependent and not nonspecific. When the contents of ET-1 and big ET-1 in the cells after culturing in the medium with or without phosphoramidon were measured, the ratio of ET-1: big ET-1 in the cells was 3.3 : 1 and phosphoramidon inverted the ratio in the cells to 1 : 3.5. These data strongly suggest that a phosphoramidon-sensitive protease converts big ET-1 to mature ET-1 intracellularly.

Animals↗
PubMed1991

Reversible reaction via a carbanion intermediate in the elimination of ammonia from L-histidine catalysed by histidine ammonia-lyase.

L-[5'-2H2]Histidine was used as a substrate to investigate the enzymatic reaction mechanism with histidine ammonia-lyase from Pseudomonas fluorescens. The study was performed to determine the exchange rate of deuterium at C-5' of the imidazole ring with solvent hydrogen relative to the net urocanic acid production. The extent of hydrogen exchange at C-5' of histidine or urocanic acid was measured by gas chromatography-mass spectrometry-selected ion monitoring, monitoring the molecular ion intensities of the respective gas chromatographic derivatives, at m/z 380 and 379 for histidine and at m/z 267 and 266 for urocanic acid. The observed hydrogen exchange at C-5' suggested a reversible mechanism via a carbanion intermediate in the reaction with histidine ammonia-lyase.

Ammonia↗
PubMed1991

Changes in responsiveness of the canine basilar artery to endothelin-1 after subarachnoid hemorrhage.

The effect of endothelin-1 (ET-1) on the basilar arteries from control and subarachnoid hemorrhage (SAH) dogs were examined. The maximal contraction of the basilar artery in response to ET-1 was markedly decreased in the SAH group. Treatment with 10(-8)M phorbol 12-myristate 13-acetate (PMA) reduced the contractile responses to ET-1 in the basilar arteries from control dogs. ET-1-induced contractions of the basilar arteries from control dogs were similar to those in strips from SAH dogs by the treatment with 10(-8) M PMA. Ca(2+)-induced contraction of the basilar arteries which were depolarized with isotonic K+ (64 mM) were significantly attenuated in SAH dogs. Treatment with PMA also reduced the contractile responses to Ca2+ in the basilar arteries from control dogs. These results indicate that decreased contractile responses of the basilar arteries to ET-1 and Ca2+ in the SAH group may be related to changes in the activity of the protein kinase C in vascular smooth muscle.

Animals↗
PubMed1991

Streptozotocin-induced diabetes in mice reduces the nociceptive threshold, as recognized after application of noxious mechanical stimuli but not of thermal stimuli.

We report herein that streptozotocin (STZ)-induced diabetes selectively alters the nociceptive threshold with respect to noxious mechanical stimuli. Mice were rendered diabetic by an injection of STZ (200 mg/kg, IV). In the tail-pinch test, the latency of the biting response to forceps was significantly decreased in animals with diabetes of 2 weeks and 8 weeks duration as compared to that in age-matched controls. However, the nociceptive threshold, as determined by the tail-flick test, was not significantly altered. The level of substance P in the spinal cord was significantly increased in mice that has been diabetic for 2 weeks, while, there was a significant decrease, as compared to control levels, in level of substance P in mice diabetic for 8 weeks. However, the level of somatostatin was not significantly altered in mice diabetic for either 2 weeks or 8 weeks. These data suggest that STZ-induced diabetes selectively alters a neuronal system that involves substance P but not somatostatin in the spinal cord.

Animals↗
PubMed1991

Alterations in the potassium-evoked release of substance P from the spinal cord of streptozotocin-induced diabetic rats in vitro.

1. The release of SPLI evoked by high levels of K+ (50 mM) from the spinal cord of diabetic rats was greater than in the case of spinal cord from control rats. 2. Morphine (10(-5) M) significantly inhibited the K(+)-evoked release of SPLI release in both the groups. However, in spinal cord from diabetic rats, morphine reduced the K(+)-evoked release of SPLI only to the levels that were observed in material from control rats prior to treatment with morphine. 3. Glucose (20 mM) and dibutyryl cyclic-AMP (10(-4) M) significantly potentiated the K(+)-evoked release of SPLI in spinal cord from control rats. 4. These findings suggest that excessive release of SPLI from the spinal cord may be associated with the reported abnormalities in nociceptive transmission in diabetic rats, and that excessive release of SPLI may be modulated by levels of glucose and/or cyclic-AMP in the spinal cord.

Animals↗
PubMed1991

Immunoreactive endothelin in plasma of nonmammalian vertebrates.

Immunoreactive endothelin (ir-ET) was estimated in plasma of nonmammalian vertebrates, using radioimmunoassay (RIA) for endothelin-1 (ET-1). Blood samples were collected from unanesthetized animals. Plasma ET was determined by RIA after extraction. Plasma levels of ir-ET were 0.7 +/- 0.2 pg/ml (n = 6) in the hagfish Eptatretus burgeri, 4.3 +/- 0.9 pg/ml (n = 5) in the banded dogfish Triakis scyllia, 3.6 +/- 0.8 pg/ml (n = 3) in the common Japanese conger Conger myriaster, 9.6 +/- 1.4 pg/ml (n = 7) in the carp Cyprinus carpio, 6.4 +/- 0.8 pg/ml (n = 5) in the bullfrog Rana catesbeiana, 6.7 +/- 0.6 pg/ml (n = 3) in the soft-shelled turtle Trionyx sinensis japonica, and 3.3 +/- 0.6 pg/ml (n = 8) in the Japanese quail Coturnix coturnix japonica. The dilution curves of the plasma extracts from each species almost paralleled the standard curve for ET-1. Analysis of the plasma extracts of the carp by reverse-phase high-performance liquid chromatography revealed that ir-ET consisted of three components, a predominant peak being located at the elution position of synthetic ET-1. The present results demonstrate clearly that an ET-1-like substance circulates in blood of nonmammalian vertebrates, suggesting an endocrine function of the peptide in these species.

Animals↗
PubMed1991

Endothelin-like immunoreactivity in the nervous system of invertebrates and fish.

There have been no reports on the distribution of immunoreactive endothelin (ir-ET) in lower vertebrates and invertebrates, except for our previous studies on the nereid Neanthes diversicolor and the earthworm Eisenia foetida. In the present study, we found ET-like immunoreactivity in five species of invertebrates and two species of fish with antiserum against synthetic endothelin-1 (ET-1). Immunoreactive perikarya and nerve fibers were observed in the central nervous system of the slug Limax marginatus, the freshwater snail Indoplanorbis exustus, and the mussel Mytilus edulis in mollusks, the field cricket Gryllus bimaculatus in insects, and the tube tunicate Ciona intestinalis in protochordates. In the medaka, Oryzias latipes, ir-ET was found in the hypothalamoneurohypophysial system, the caudal neurosecretory system, the gill, and the kidney. Immunoreactive cells were also found in the mucous gland of the slug and in the adenohypophysis of the lamprey, Lampetra japonica. The wide distribution of ET-like substances in invertebrates and fish provides evidence for the case that ET found in mammals has a long evolutionary history.

Animals↗
PubMed1991

Effects of the R(+)- and S(-)-isomers of beta-adrenoceptor blockers with intrinsic sympathomimetic activity, befunolol and carteolol, on rabbit intraocular pressure.

Effects of the R(+)- and S(-)-isomers of befunolol and carteolol, beta-adrenoceptors with intrinsic sympathomimetic activity, on the rabbit intraocular pressure were tested. The intraocular pressure was decreased by instillation of the R(+)- and S(-)-isomers of befunolol (0.1 and 0.3%) and of carteolol (1.0%) to the eye and attained the minimum level at 60 min. However, 0.3% of the R(+)- and S(-)-isomers of carteolol did not influence the pressure. The corresponding time courses for the intraocular pressure for the R(+)- and S(-)-isomers did not differ, suggesting that in the treatment of glaucoma, the therapeutic advantage of the R(+)-isomers of befunolol and carteolol may be similar to the S(-)-isomers.

Adrenergic beta-Antagonists↗
PubMed1991

Attenuation of depressor response induced by platelet activating factor and acetylcholine in streptozotocin-induced diabetic rats.

The in vivo and in vitro effects of platelet-activating factor (PAF, 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphorylcholine) and acetylcholine (ACh) on vascular relaxation responses were examined in streptozotocin-induced diabetic rats. Intravenous injection of PAF and ACh (0.03 to 10 micrograms/kg) decreased the mean blood pressure in both control and diabetic rats in a dose-dependent fashion. Initial blood pressure in diabetic rats did not significantly differ from that in control rats. However, depressor responses induced by PAF and ACh in diabetic rats were attenuated more than those in control rats. In perfused mesenteric arterial bed preconstricted with methoxamine (10(-5) - 10(-4) M), PAF (10(-11) -3 x 10(-10) M) produced a concentration-dependent relaxation. However, this relaxation was significantly attenuated in the diabetic preparation compared with the control preparation. ACh also produced a concentration-dependent vasodilation in perfused mesenteric arterial bed. The concentration-response curve for the relaxation of the mesenteric arterial bed to ACh in diabetic preparation was shifted to the right compared with that in control preparation. A pretreatment with oxyhaemoglobin (10(-6) M) also shifted the concentration-response curves for relaxation to ACh in both control and diabetic preparation to the right. There was no difference in relaxation induced by sodium nitroprusside between the diabetic and the control preparation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Effects of L-tryptophan on the development of tolerance to the antitussive effects of dihydrocodeine.

The effects of L-tryptophan on the development of tolerance to the antitussive effects of dihydrocodeine were examined in rats. Chronic co-administration of L-tryptophan with dihydrocodeine prevented the development of tolerance to the antitussive effects of dihydrocodeine. Furthermore, the antitussive effects of dihydrocodeine in dihydrocodeine-tolerant rats were fully restored by acute co-administration of L-tryptophan, as evidenced by a decrease of about 50% in the ED50 value of dihydrocodeine. Thus, it is concluded that L-tryptophan may antagonized the development of tolerance to the antitussive effects of dihydrocodeine.

Animals↗
PubMed1991

Effects of muscarinic antagonists on experimental nasal secretion in guinea pigs.

The effects of muscarinic antagonists on acetylcholine (ACh)- and histamine-induced nasal secretion were investigated in guinea pigs. Inhalations of flutropium (0.01 to 0.3%) and atropine (0.03 to 0.3%) into the nasal cavities dose-dependently inhibited the nasal secretion induced by ACh. The inhibitory action of flutropium was slightly stronger than that of atropine. Inhalations of pirenzepine (0.3%) and gallamine (0.3%) had no effect on the ACh-induced nasal secretion. However, 4-DAMP dose-dependently inhibited the nasal secretion induced by ACh. Inhalations of flutropium (0.3%) and diphenhydramine (0.3%) showed a similar inhibitory action on the histamine-induced nasal secretion. These results suggest that 1) inhalation into the nasal cavities of flutropium was effective in experimental model of ACh- and histamine-induced nasal secretion, 2) M3-cholinergic receptors may be dominant in the nasal secretion induced by ACh and 3) the experimental model of drug-induced nasal secretion in guinea pigs used in the present study can be employed to develop therapeutic drugs for nasal secretion.

Acetylcholine↗