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Volume 66 (1994)
- Issue 4 Pages 397-
- Issue 3 Pages 281-
- Issue 2 Pages 167-
- Issue 1 Pages 1-
Volume 66, Issue 2
Displaying 1-15 of 15 articles from this issue
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Toshio Nakaki, Ryuichi Kato1994 Volume 66 Issue 2 Pages 167-171
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSL-Arginine is an essential amino acid for infants and growing children. This amino acid is a substrate for at least five enzymes identified in mammals, including arginase, arginine-glycine transaminase, kyotorphine synthase, nitric oxide synthase (NOS) and arginine decarboxylase. L-Arginine exerts antihypertensive and antiproliferative effects on vascular smooth muscles. NOS and arginine decarboxylase appear to be important for the effect of L-arginine on the circulatory system, since each produces nitric oxide (NO), a potent vasodilator, and agmatine, an endogenous noncatecholamine ligand for central alpha-2 adrenoceptors, from L-arginine. Several issues must be clarified before the mechanisms by which L-arginine exerts its effects on the circulatory system can be fully understood.View full abstractDownload PDF (361K) -
Shigekatsu Kohno, Shintaro Nakao, Kohji Ogawa, Hideki Yamamura, Takesh ...1994 Volume 66 Issue 2 Pages 173-180
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSAnaphylactic histamine release from isolated rat peritoneal mast cells was concentration-dependently blocked by a 5-min treatment with exogenous histamine at 0.9 and 9 μM and enhanced by a 20- to 30-min treatment with thioperamide (H3-antagonist) at 3 μM with significance, but little affected by mepyramine (H1-antagonist) and cimetidine (H2-antagonist) at the cell concentration of 106 mast cells/ml. At a low concentration of mast cells (104 mast cells/ml), (R)-α-methylhistamine (α-MH), an H3-agonist, at 0.9-90 μM also inhibited the release in a concentration-dependent fashion. Thioperamide, but neither mepyramine nor cimetidine, significantly restored the decreased release by α-MH. However, the complete restoration by thioperamide could not be achieved because the drug itself slightly but concentration-dependently inhibited anaphylactic histamine release. On the other hand, not only betahistine and dimaprit but also α-MH did not suppress histamine release from the mast cells induced by compound 48/80. In rat plasma, considerable levels of histamine were detected. From these results, it is strongly suggested that histamine H3-like receptors are largely responsible for the negative feedback regulation of the anaphylactic histamine release from rat peritoneal mast cells.View full abstractDownload PDF (529K) -
Kiyoyuki Kitaichi, Kiyofumi Yamada, Takaaki Hasegawa, Hiroshi Furukawa ...1994 Volume 66 Issue 2 Pages 181-189
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSIn this study, we investigated whether risperidone, a serotonin-S2A (5-HT2A)/dopamine-D2 (D2)-receptor antagonist, inhibits phencyclidine (PCP)-induced stereotyped behaviors in comparison with haloperidol and ritanserin. Moreover, we also attempted to investigate the effects of these antipsychotics on the contents of dopamine, serotonin (5-HT) and their metabolites in rat striatum and frontal cortex. In rats, PCP (5 mg/kg, i.p.) caused hyperlocomotion and stereotyped behaviors, including sniffing, head-weaving, backpedalling and turning. Both risperidone (0.8-2.4 mg/kg, p.o.) and haloperidol (0.3-1.0 mg/kg, p.o.) inhibited these behaviors, except for backpedalling, in a dose-dependent manner. PCP (10 mg/kg, i.p.) produced hyperlocomotion and stereotyped behaviors, including rearing, sniffing head-twitch, backpedalling and turning. Risperidone (0.8-2.4 mg/kg, p.o.) inhibited both hyperlocomotion and PCP-induced behaviors, except for backpedalling, while ritanserin (3-10 mg/kg, p.o.) inhibited only the head-twitch. These results suggest that risperidone may have an antipsychotic effect on schizophrenia as well as PCP psychosis in humans by exerting a mixed 5-HT2A/D2 antagonism. Neurochemically, the increasing effects of risperidone on the content of DOPAC and the ratio of DOPAC to dopamine in the striatum were lower than those of haloperidol. These findings may support the view that the extrapyramidal side effects of risperidone are lower than those of haloperidol in clinical situations.View full abstractDownload PDF (661K) -
Ikunobu Muramatsu, Shigeru Kigoshi, Yasuo Oda1994 Volume 66 Issue 2 Pages 191-193
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSElectrical transmural stimulation of isolated iris dilator muscle of the rabbit produced a transient contraction that consisted of adrenergic and nonadrenergic components. In contrast to the adrenergic component, the nonadrenergic component was resistant to prazosin and other adrenoceptor antagonists. However, both components were completely blocked by guanethidine or tetrodotoxin. Among some tested compounds including neuropeptide Y, both ATP and 2-methylthio ATP produced a transient contraction in the dilator muscle and the sustained treatment with each markedly attenuated the nonadrenergic responses to electrical stimulation and to ATP. Suramin had no effect on and α, β-methylene ATP potentiated the responses to electrical stimulation and to ATP. These results suggest that the nonadrenergic contraction induced by electrical transmural stimulation is a sympathetic purinergic response that may be mediated through unique purinoceptors.View full abstractDownload PDF (185K) -
Koji Matsuda, Junken Aoki, Masaatsu K. Uchida, Tamiko Suzuki-Nishimura1994 Volume 66 Issue 2 Pages 195-204
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe N-acetyl glucosamine (GlcNAc)-specific lectin Datura stramonium agglutinin (DSA) rapidly and sugar-specifically released histamine from rat peritoneal mast cells, and pertussis toxin (IAP) inhibited it, suggesting that DSA activated mast cells via an IAP-sensitive G protein pathway. The additive effects of DSA and basic secretagogues such as compound 48/80 that activate IAP-sensitive G protein directly suggest that they shared the same mechanism of action including involvement of the IAP-sensitive G protein. Using lectin-blotting, blots of the corresponding glycoproteins detected by DSA diminished by haptenic sugar or pretreatment of the cells with N-glycosidase F, suggesting that the binding of DSA was responsible for the mast cell activation. The other GlcNAc-specific lectins such as Phytolacca americana mitogen, Solanum tuberosum agglutinin and wheat germ agglutinin (WGA) inhibited the histamine release induced by DSA, suggesting that these lectins were antagonists, but DSA was an agonist. Sialic acid-specific Macckia amurensis mitogen (MAM) inhibited the histamine release, and neuraminidase-treatment decreased mast cell activation induced by DSA. At least four mast cell glycoproteins that have affinity to DSA, WGA and MAM and are sensitive to neuraminidase-treatment were detected by lectin-blotting. Some of them may be binding sites coupled to histamine release including the IAP-sensitive G protein pathway. DSA is a useful tool for studying signal transduction of mast cells including the involvement of the IAP-sensitive G protein.View full abstractDownload PDF (749K) -
Tamiko Suzuki-Nishimura, Tadahide Furuno, Masaatsu K. Uchida, Mamoru N ...1994 Volume 66 Issue 2 Pages 205-211
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSA confocal fluorescence microscope using fluo-3 and 9-(dicyanovinyl)-julolidine (DCVJ) was used to study the mast cell activation by the N-acetyl glucosamine oligomer specific lectin Datura stramonium agglutinin (DSA) and inhibition by antagonist lectins having affinity to N-acetyl glucosamine (GlcNAc). DSA induced a transient increase in intracellular free calcium concentration ([Ca2+]i) followed by cytoskeletal disassembly and reassembly in rat peritoneal mast cells. These changes induced by DSA resulted in histamine release. The time course of fluorescence intensity in mast cells loaded with fluo-3 or DCVJ and activated by DSA resembled those activated by the basic polymer compound 48/80. Inhibition of [Ca2+]i rise by antagonist lectins was responsible for the inhibition of cytoskeletal assembly and the consequent histamine release induced by DSA. At the level of the individual cell, a mast cell stimulated by DSA responds in an all-or-none fashion. DSA possibly induced intracellular calcium mobilization and cytoskeletal change by recognizing the GlcNAc-oligomer residues of specific glycoproteins of mast cells.View full abstractDownload PDF (485K) -
Katsuo Koike, Issei Takayanagi, Midori Muramatsu, Shin-ichi Ohki, Taka ...1994 Volume 66 Issue 2 Pages 213-220
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSβ-Adrenoceptors in the guinea pig taenia caecum were investigated by measuring relaxation responses to agonists and by a radioligand binding assay using [3H]CGP 12177. The rightward shift of the isoprenaline concentration-response curve was observed by butoxamine, a β2-selective antagonist, and the pA2 value for butoxamine was 6.46. In control preparations, catecholamines caused relaxation with the following rank order of potency: isoprenaline > adrenaline > noradrenaline. However, in the presence of 10-6 M phentolamine, 3 × 10-4 M atenolol and 10-4 M butoxamine, the rank order of potency of the agonists was: isoprenaline > noradrenaline > adrenaline. CGP 12177 caused graded relaxation of the guinea pig taenia caecum, and this response was not influenced by 10-6 M phentolamine, 3 × 10-4 M atenolol, 10-4 M butoxamine or 10-6 M propranolol. The Scatchard plot of the specific [3H]CGP 12177 binding to microsomal fractions from the guinea pig taenia caecum showed two affinity sites of the receptor: high affinity (KD=0.64 nM) and low affinity (KD=142.21 nM) sites. The pKD value of the high affinity site of [3H]-CGP 12177 was in agreement with its pA2 value, and that of the low affinity site was in agreement with its pD2 value. These results suggest that isoprenaline-, noradrenaline- and adrenaline-induced relaxations of the guinea pig taenia caecum predominantly involve β2- and β3-adrenoceptors, whereas CGP 12177-induced relaxation is mediated solely through β3-adrenoceptors.View full abstractDownload PDF (539K) -
Mamoru Saito, Satoshi Homma, Isao Yamatsu, Masaaki Sato, Norio Ohshima1994 Volume 66 Issue 2 Pages 221-229
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe aim of the present study was to visualize the superficial glomeruli of the Munich-Wistar (MW) rat and to characterize the responses of the renal microvasculature to endothelin-1 (ET-1). We first examined the distribution of superficial glomeruli of the MW rat compared to that in a control strain (Wistar rat). Secondly, we examined the effects of ET-1 on the renal microcirculation of the MW rat. The right kidney was perfused with a Krebs-Ringer solution containing fluorescein isothiocyanate dextran (FITC-dextran) and was visualized under an epi-illuminated fluorescence microscope system. Changes in perfusion pressure and diameter of the microvessels accompanying the administration of ET-1 (10 fmole-300 pmole) were measured. The number of superficial glomeruli was greater in the MW rat than in the Wistar rat. ET-1 had long-lasting and dose-dependent pressor effects. Perfusion pressure showed a 3.5-fold increase compared with the control, and the afferent arterioles showed greater dose-dependent vasoconstriction than the efferent arterioles. These findings suggest that the MW rat is a useful animal model for the study of renal microcirculation and that the renal microcirculation is extremely sensitive to ET-1.View full abstractDownload PDF (796K) -
Toshihisa Fujiwara, Hirofumi Yuasa, Noriko Ogiku, Yoshiaki Kawai1994 Volume 66 Issue 2 Pages 231-240
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSOur previous studies showed that imidapril prevented the occurrence of cerebral stroke and ameliorated biochemical parameter changes of renal dysfunction at a dose that did not inhibit the progression of hypertension in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). To confirm these findings, a histopathological investigation was conducted on the kidney of salt-loaded (from 11 to 16 weeks of age) SHRSP, which was the subject of the preceding study. Their brains and hearts were also examined. Histopathologically, renal lesions such as fibrinoid necrosis and proliferative arteritis of small calibration arteries, necrotizing glomerulitis and tubular degeneration, and cerebral hemorrhage and slight cardial hypertrophy were observed in salt-loaded control SHRSP. The occurrence of these lesions were prevented in a dose-dependent manner by the administration of imidapril (1 and 2 mg/kg/day). Especially, the preventive effects on the renal lesions were apparently noted. Enalapril also prevented these renal lesions, but its preventive effects were weaker than those of imidapril at the same dose (2 mg/kg/day). It became evident from the results of the present and previous studies that imidapril reduced renal biochemical and histopathological injuries.View full abstractDownload PDF (1019K) -
Hiromi Tsushima, Mayumi Mori, Tomohiro Matsuda1994 Volume 66 Issue 2 Pages 241-246
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSWe investigated the effects of angiotensin II (Ang II), microinjected into the supraoptic (SON) and paraventricular (PVN) nuclei of rats, on the urine outflow rate and underlying mechanisms. Ang II produced antidiuretic effects in a dose-dependent manner with ED50 values of 0.1 and 0.05 nmol in the SON and PVN, respectively. [Sar1, Ile8]Ang II at 0.1 nmol diminished the Ang II (0.5 nmol)-induced anti-diureses in the SON more markedly than in the PVN. A high dose of [Sar1, Ile8]Ang II, 1 nmol, completely inhibited the effects in both the nuclei. In addition, the Ang II (1 nmol)-induced antidiuretic effects were partially inhibited by phenoxybenzamine (80 nmol) in the SON and by phenoxybenzamine, timolol (100 nmol) and propranolol (100 nmol) in the PVN. The microinjection of Ang II (1 nmol) into both the nuclei, after pretreatment with a vasopressin V1V2-antagonist, d(CH2)5-D-Tyr(Et)VAVP (i.v.), significantly increased the urine outflow rate. These findings suggest that 1) Two mechanisms account for the Ang II receptor mediated antidiureses resulting from an increase in vasopressin release: direct stimulation on vasopressin-containing neurons and indirect stimulation on them through α-adrenoceptors in the SON and α- and β-adrenoceptors in the PVN; 2) The Ang II-induced antidiuretic effect in the SON is slightly less potent than that in the PVN; and 3) Ang II receptors in the nuclei may possibly produce the diureses through mechanisms that are not presently understood.View full abstractDownload PDF (451K) -
Fumie Yufu, Toru Egashira, Yasumitsu Yamanaka1994 Volume 66 Issue 2 Pages 247-255
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSTo evaluate whether any degenerative changes affect the brain cholinergic systems during natural aging, we compared various cholinergic biochemical markers (number of muscarinic receptors, mAChR; choline acetyltransferase activity, ChAT; acetylcholinesterase activity, AChE; and sodium-dependent high affinity choline uptake) in the cortical (CR) and subcortical (SS) regions of the brains of aged (24 month) and young (2 month) rats. Using [3H]-quinuclidinyl benzilate ([3H]-QNB) as the ligand of muscarinic receptor binding, the numbers of mAChR decreased about 30% in both the CR and the SS of aged rats compared with those in young rats, while a significant age-related increase in the affinity of mAChR was observed. [3H]-QNB binding in both the young and aged rat brain was displaced markedly by pirenzepine, while [3H]-QNB binding in the SS of the aged rat brain was displaced at low concentrations of atropine. The Vmax values of ChAT and AChE also decreased about 20-30% compared with those of young rats. The sodium-dependent high affinity choline uptake was lower in the crude synaptosomal fraction prepared from aged rat brain than in young brain. Hemicholinium-3 inhibited the choline uptake in young rat brain at a concentration range of 1 μM - 10 nM, but choline uptake in aged brain was insensitive to hemicholinium-3. These results indicate that natural aging brings about a diffuse and multiple depletion of various biochemical markers in cholinergic neurons.View full abstractDownload PDF (623K) -
Shiroh Kishioka, Shigeru Nishida, Yuko Fukunaga, Hiroyuki Yamamoto1994 Volume 66 Issue 2 Pages 257-263
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSElevation of plasma corticosterone (PCS) has been used as an indicator of morphine withdrawal, but it is not clear whether the magnitude of elevation is related to the intensity of the dependence. The dose-dependent effects of naloxone on PCS and body weight were studied in male Sprague-Dawley rats rendered physically dependent on morphine by injecting increasing doses of 40-120 mg/kg/day, s.c. twice daily for 1-6 days. Naloxone (0.01-2.0 mg/kg, s.c.) was administered 3 hr after the last morphine administration. Naloxone elevated PCS levels in a dose-dependent manner in all groups treated with morphine, and the elevation was correlated with the number of days of morphine treatment. Naloxone also reduced dose-dependently the body weight in all groups treated with morphine; in this case, a reverse correlation was obtained between the body weight changes and the PCS levels. It was confirmed that PCS elevation is a quantitative sign of naloxone-precipitated morphine withdrawal and that the elevation is indicative of the degree of morphine physical dependence.View full abstractDownload PDF (469K) -
Hiroko Itoh, Hitoshi Ito, Hideomi Amano, Hiroyuki Noda1994 Volume 66 Issue 2 Pages 265-271
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSThe effects of F III-2-b (Agaricus blazei Murill polysaccharide) with or without 5-fluorouracil (5-FU) on immune responses were investigated in Meth A tumor-bearing and normal mice. The i.p. administration of F III-2-b (10 mg/kg/day × 30) moderately inhibited the growth of Meth A tumor cells implanted s.c. in mice. Development of implanted tumors was strongly inhibited by the combination of F III-2-b and 5-FU. The picryl chloride-induced delayed type hypersensitivity (PC-DTH) response in mice was depressed after the implantation of tumor and treatment with 5-FU. F III-2-b restored the suppression of PC-DTH by 5-FU, but did not increase the PC-DTH of normal mice. F III-2-b not only enhanced the degree of spleen cell-mediated sheep red blood cells (SRBC) hemolysis (quantitative hemolysis of SRBC), the indexes of the spleen and thymus, and the number of spleen cells but also restored the suppressive effect of 5-FU. In the group receiving F III-2-b, the percentages of splenic Thy1.2-, L3T4- and asialo GM1-positive cells were significantly increased as compared with the tumor-bearing mice treated with saline. Furthermore, the L3T4+/Lyt2+ ratio showed a tendency to increase, and the Lyt2+/Thy1.2+ ratio was markedly decreased. These results suggest that the antitumor effect of F III-2-b may be correlated with the changing pattern of the Thyl.2-, L3T4- and asialo GM1-positive cells.View full abstractDownload PDF (538K) -
Kazuyuki Shibata, Shigeo Kitayama, Katsuya Morita, Masaharu Shirakawa, ...1994 Volume 66 Issue 2 Pages 273-276
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESS12-O-Tetradecanoylphorbol-13-acetate (TPA) time-dependently inhibited the platelet-activating factor (PAF)-induced rise in cytosolic free calcium concentration ([Ca2+]i) in rabbit neutrophils, whereas staurosporine significantly enhanced it. Inositol 1, 4, 5-trisphosphate (IP3) induced Ca2+ release in digitonin-permeabilized cells but not in PAF-pretreated permeabilized cells. IP3-induced Ca2+ release was not affected by protein kinase C activators or inhibitors. In the cells pretreated with PAF and thapsigargin in Ca2+-deficient medium, stimulated Ca2+ entry was evoked by the subsequent addition of CaCl2. TPA inhibited the Ca2+ entry induced by PAF and thapsigargin in a staurosporine-reversible manner but not thapsigargin-induced [Ca2+]i elevation. These results suggest that protein kinase C negatively regulates PAF- and thapsigargin-induced rise in [Ca2+]i possibly by inhibiting Ca2+ store depletion-induced Ca2+ entry.View full abstractDownload PDF (277K) -
A.F.M. Mohibur Rahman, Masakatsu Takahashi, Hiroshi Kaneto1994 Volume 66 Issue 2 Pages 277-280
Published: 1994
Released on J-STAGE: April 10, 2006
JOURNAL FREE ACCESSPain associated-anxiety induced by formalin, which resulted in a significant delay in the development of tolerance to morphine antinociception, failed to prevent the development of physical dependence as evidenced by naloxone challenge. Dependence also developed in mice rendered tolerant to morphine. Thus, the development of morphine dependence was observed in the absence and presence of tolerance to morphine antinociception; Our results further confirm the dissociation of opioid tolerance and dependence in the animal model of experimental pain/anxiety.View full abstractDownload PDF (221K)
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