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Volume 45 (1987)
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Volume 45, Issue 1
Displaying 1-16 of 16 articles from this issue
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Tadashi NAGAMATSU, Yoshio SUZUKI1987 Volume 45 Issue 1 Pages 1-6
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSWe investigated the effects of prostaglandin E1 (PGE1) and dipyridamole on the disposal of macromolecules via mesangial channels to understand the antinephritic effect of PGE1. To increase glomerular carbon, rats were injected i.v. first with anti-glomerular basement membrane (GBM) serum and then with 30 mg/100 g body weight of carbon. Carbon in the glomerulus was detected with an image analyzer. Administration of anti-GBM serum resulted in about a 2 to 3-fold increase in glomerular uptake of carbon in the normal rats. To investigate the day-to-day situation of glomerular carbon, the right kidney was removed the day after carbon injection, and the left kidney was isolated on days 7, 14 and 21. By day 21, glomerular carbon had decreased significantly. Rats with carbon received PGE1 0.1×2 and 1.0×2 mg/kg, s.c., and dipyridamole 200 and 400 mg/kg, p.o., for 10 days after the isolation of the right kidney. PGE1 administration did not cause a decrease in the amount of glomerular carbon compared with that of the control. However, the dipyridamole group showed a more rapid decrease of glomerular carbon. It is concluded that PGE1 has no effect on the mesanigial channels, but dipyridamole can accelerate the disposal of glomerular carbon by way of the mesangial channels.View full abstractDownload PDF (433K) -
Yasushi KANAI, Norio OHNUMA, Hisayuki MATSUO1987 Volume 45 Issue 1 Pages 7-13
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSLocalization of binding sites for synthetic rat atrial natriuretic polypeptide (α-rANP) and the effect of the peptide on net water and electrolyte movement in vivo perfused small intestine of the rat were studied. Autoradiographic study demonstrated that specific binding sites were localized on a space between the base of epithelia and lamina propria of the small intestine. Alpha-rANP (0.25 μg/min) infused into the superior mesenteric artery of rats increased net absorption of water (46% increase in comparison with controls), Na (84% increase) and Cl (70% increase) across the small intestinal tract perfused with Ringer's solution. These increases were also observed when glucose-free Ringer's solution was employed. Thus it would be concluded that the Na-glucose cotransport system is not involved in the action of α-rANP. These observations suggest that α-rANP controls circulating water-electrolyte balance through regulating not only renal function but also intestinal water, Na and Cl absorption.View full abstractDownload PDF (413K) -
Kouichi AKAHANE, Kazuhisa FURUHAMA, Fujiroh INAGE, Takeshi ONODERA1987 Volume 45 Issue 1 Pages 15-25
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSRats developed anemia during treatment with high doses of malotilate, a hepatotropic agent. A repeated dose of 1, 000 mg/kg caused a 20-30% decrease in the number of red blood cells and in hematocrit and hemoglobin values within the first week. In response to the anemia, the reticulocyte count increased, and target cells, acanthocytes and Howell-Jolly bodies appeared in the peripheral blood. In the spleen, hemosiderin deposition was enhanced. The life span of 51Cr-label led erythrocytes was shortened from 15 to 2 days in the high-dose group, whereas plasma iron disappearance and hemoglobin synthesis were significantly potentiated. Hemorrheological examinations revealed an increase in blood viscosity. Hemolytic resistance to mechanical stimuli was reduced, but that to osmotic stimuli was enhanced. At the same time as the onset of the anemia, serum and red cell membrane cholesterol and phospholipid began to increase on day 4 or 6. Incorporation of cholesterol into red cell membranes in vitro was significantly potentiated when serum obtained from rats after a single administration of 1, 000 mg/kg was added to the culture. These results suggest that malotilate causes an increase in the surface area of the erythrocytes by accelerating the incorporation of cholesterol into their membranes, and such erythrocytes might be rheologically impaired and captured more easily by the spleen.View full abstractDownload PDF (553K) -
Hirohiko SAKAMOTO, Nobuharu YOKOYAMA, Takashi NISHIMOTO, Kazuyuki MURA ...1987 Volume 45 Issue 1 Pages 27-36
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe binding characteristics of [3H]quinupramine to rat brain membrane fractions were studied. The specific binding of [3H]quinupramine to rat brain membrane fractions was stable, reversible and saturable. Scatchard analysis of the data from saturation experiments indicated that the specific binding was a single population with an affinity (KD) of 3.04 nM, a maximal binding site number (Bmax) of 714 fmol/mg protein, and a Hill coefficent (nH) of 1.08. Compounds known to inhibit muscarinic cholinergic receptors such as atropine and quinuclidinyl benzilate were the most potent competitors of [3H]quinupramine binding. When the drug potencies in inhibiting [3H]quinupramine binding were tested in the presence of 10 nM atropine, mianserin was the most potent competitor. Studies of the subcellular fractions showed that there was an enrichment of [3H]quinupramine binding sites in the synaptosome fraction. The regional distribution study revealed the highest densities of binding sites in the cerebral cortex and the lowest in the cerebellum. Thus, the specific binding of [3H]quinupramine observed here can be accounted for by both muscarinic cholinergic and serotonin S2 receptors.View full abstractDownload PDF (542K) -
Yukio YONETANI, Kazumi IWAKI, Yasunao OGAWA1987 Volume 45 Issue 1 Pages 37-43
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSBoth potassium oxonate and allantoxanamide have been reported as useful reagents for inhibiting urate oxidase, with the hyperuricemic effect of allantoxanamide being longer-lasting than that of oxonate in rats. The present study was done to evaluate the utility of allantoxanamide for investigating problems concerning hyperuricemia using rats. A single intraperitoneal administration of 1 50 mg/kg allantoxanamide elevated the plasma uric acid level progressively during the experiment for 6 hr, resulting in a much higher level than that maintained by means of repeated dosing with 250 mg/kg potassium oxonate, i.p., at 2-hr intervals. Such a severe and long-lasting hyperuricemia caused by allantoxanamide was due to decreased renal function of uric acid excretion according to its nephrotoxicity in addition to the inhibition of urate oxidase like that by oxonate. Thus, we concluded that allantoxanamide might be a useful reagent for investigating the causes of hyperuricemia with renal failure, but was not a practical agent like oxonate in order to evaluate the response to uricosuric agents.View full abstractDownload PDF (379K) -
Hitoshi KONTANI, Yoichi KAWABATA, Ryozo KOSHIURA1987 Volume 45 Issue 1 Pages 45-53
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSWe studied the effects of the γ-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 μg 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.View full abstractDownload PDF (505K) -
Kei TSUZURAHARA, Setsuko ISHIKAWA, Yasutoshi ONO, Takashi MURATA, Mats ...1987 Volume 45 Issue 1 Pages 55-62
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSMechanism of the antiallergic action of 6-methyl-N-(1H-tetrazol-5-yl)-2-pyridinecarboxamide (TA-5707F) was studied using the water-soluble sodium salt (TA-5707). 1) TA-5707 administered p.o. at the dose ca. 3 times the ID50 for the PCA reaction did not inhibit capillary dye leakage induced on the rat skin by intracutaneous injection of histamine, serotonin, bradykinin and leukotriene D4 (LTD4). 2) TA-5707, at concentrations above 10-7 M, inhibited antigen-induced histamine release and dye leakage in the rat peritoneal cavity (passive peritoneal anaphylaxis). 3) TA-5707 inhibited both anaphylactic and compound 48/80-induced histamine release from the rat peritoneal mast cells, the IC50 being ca. 10-5 M in both cases. It was concluded that TA-5707F exerts its antiallergic action by inhibiting the release of chemical mediators from sensitized cells.View full abstractDownload PDF (391K) -
Miwa MISAWA, Kiyoteru TAKENOUCHI, Toichi ABIRU, Yasushi YOSHINO, Saizo ...1987 Volume 45 Issue 1 Pages 63-68
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSA new rat asthma model was devised, and with the model, allergic bronchoconstrictor responses and effects of disodium cromoglycate (DSCG) were compared among Wistar, Lewis and Fischer 344 rats. Rats were actively sensitized with DNP-Ascaris antigen (DNP-As) and killed Bordetella pertussis vaccine. After eight days, asthmatic response was provoked by inhalation of DNP-As. The bronchomotor reponse was measured with a modified Konzett-Rossler method in diaphragm-sectioned rats. The inhalation of DNP-As using a newly devised apparatus caused a marked asthmatic response with negligible effects on systemic blood pressure and heart rate. The extent of the bronchoconstriction provoked was of the following order: Wistar>Lewis≈ Fischer 344. There was no relationship between the individual 48 hr PCA titer and the bronchoconstriction that occurred in any strain of rats. The bronchoconstrictions were inhibited by DSCG (10 mg/kg, i.v.) and the inhibition ratios were 28%, 36% and 33% in Wistar, Lewis and Fischer 344 rats, respectively. The inhibitions were statistically significant in the latter two strains. Fischer 344 rats were more susceptible to the damage resulting from the operative procedures. The above findings suggest that Lewis rats are the most suitable among the above strains as a model for studying the effects of antiallergic agents.View full abstractDownload PDF (350K) -
Kenzo TAKAGI, Tatsuo SATAKE, Takaaki HASEGAWA, Kenichi MIYAMOTO, Shiny ...1987 Volume 45 Issue 1 Pages 69-77
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSAt non-cytotoxic concentrations, actions of smooth muscle relaxants except for the action of isoproterenol (IPN) on the effect of vinblastine (VBL) and mitomycin C (MMC) in rat ascites hepatoma AH66 cells resistant to these antitumor agents clearly separated into two groups. I PN hardly influenced the effects of both VBL and MMC. Although verapamil, a calcium-antagonist, and W-7, a calmodulin inhibitor, enhanced the growth-inhibitory effect and uptake of VBL by inhibiting the VBL efflux, these drugs did not influence the effect and uptake of MMC. In contrast, forskolin, an adenylate cyclase activator, db-cAMP, a cAMP analog, and theophylline, a cyclic nucleotide phosphodiesterase inhibitor, potentiated the effect of MMC, but did not influence the effect of VBL. The combination effect of forskolin and db-cAMP might be elucidated from the increase of inward transport of MMC through the action of the intracellular cAMP elevated by these drugs. Theophylline, however, only slightly increased both intracellular cAMP level and MMC uptake into the cells, similar to the action of IPN. We thought that the combination effect of theophylline was effected through its other activity of repair inhibition against AH66 cells, which are resistant to MMC due to their high capacity to repair impaired DNA. Thus, the smooth muscle relaxants used in this study enhanced the growth-inhibitory effect of a distinct antitumor agent through their individual activity against tumor cells.View full abstractDownload PDF (447K) -
Toru EGASHIRA, Toshinori YAMAMOTO, Yasumitsu YAMANAKA1987 Volume 45 Issue 1 Pages 79-88
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSA and B form MAO activities in mitochondria and synaptosome were measured in the brain of monkeys administered d-methamphetamine (d-MP) 2 mg/kg, i.m., daily for 7 days. When mitochondria were used as an enzyme preparation, the Km and Vmax values decreased with 5-HT (serotonin for A-form MAO substrate) and β-phenylethylamine (β-PEA for B-form MAO substrate), while in the synaptosome, a significant increase of the Km and Vmax values was observed with 5-HT and dopamine as substrates. The mitochondrial MAO treated with d-MP was inhibited strongly by clorgyline and deprenyl with, β-PEA as a substrate, while synaptosomal MAO was highly sensitive to these MAO inhibitors with 5-HT as a substrate. MP and amphetamine (AP) were found in brain mitochondrial and synaptosomal preparations of monkeys administered 2 mg/kg d-MP, i.m. daily for 7 days; MP and AP contents were 5.05±0.22 pg/mg protein and 37.3±3.8 ng/mg protein in mitochondria and 2.35±0.35 pg/mg protein and 46.4±1.5 ng/mg protein in synaptosomes, respectively. MAO was inhibited by MP and its metabolites, AP, p-hydroxymethamphetamine (OH-MP) and p-hydroxyamphetamine (OH-AP), with 5-HT, , β-PEA and dopamine as substrates, in vitro. MP and its metabolites were more potent inhibitors of A-form MAO than B-form MAO.View full abstractDownload PDF (512K) -
Ken NAKAZAWA, Yutaka KASUYA, Koki SHIGENOBU1987 Volume 45 Issue 1 Pages 89-95
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of phenylephrine on contraction and Ca-action potentials were investigated to clarify whether the α-adrenergic mechanism may play a role in chick ventricles. Phenylephrine increased the contractile force of the ventricles isolated from both embryonic and hatched chicks, while methoxamine did not affect their contractility. Developmental changes in the sensitivity to phenylephrine, i.e., increase with age from late embryonic to early neonatal stages, were quite similar to those to a β-agonist, isoproterenol. The positive inotropism of phenylephrine was antagonized by phentolamine and sotalol, but not antagonized by prazosin or yohimbine. Isobutylmethylxanthine augmented the effect of phenylephrine. Maximum upstroke velocity of Ca-action potentials recorded in partially depolarized ventricles were enhanced by phenylephrine, and the enhancement was eliminated by sotalol but not by phentolamine. The results suggested that the β-adrenergic action of phenylephrine may be involved in part of its positive inotropic effect, which is mediated by increased Ca-influx through sarcolemma. Another mechanism may also participate in the effects of phenylephrine, but may not necessarily be classified as an “α-adrenergic effect”.View full abstractDownload PDF (320K) -
Akira TANAKA, Shuichiro NISHIHARA, Tadashi MISAWA, Hiroshi IBAYASHI1987 Volume 45 Issue 1 Pages 97-105
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESS3H-Cimetidine binding to plasma membranes of isolated guinea pig gastric glands was investigated, and the effects of five H2-receptor antagonists on 3H-cimetidine binding and histamine stimulation of cellular cAMP were compared. Of the five cations tested, Cu++ markedly increased specific 3H-cimetidine binding. 3H-Cimetidine had high affinity (Kd=0.41×10-6M) and low affinity (Kd=12.8×10-6M) binding sites. Cimetidine and etintidine were potent inhibitors of 3H-cimetidine binding, while famotidine, ranitidine and TZU-0460 were not. Histamine stimulation of cellular cAMP was competitively inhibited by H2-receptor antagonists yielding pA2 values of 6.41 for cimetidine, 6.82 for etintidine, 6.87 for ranitidine, 6.94 for TZU-0460 and 7.60 for famotidine. Because the KB value (log KB=-pA2) of 0.39×10-6M for cimetidine is close to the Kd value for the high affinity 3H-cimetidine binding site, it is presumed to represent a part of the H2-receptor, and the relative potency of etintidine against cimetidine in inhibiting 3H-cimetidine binding is similar to that in inhibiting histamine stimulation of cellular cAMP. These results suggest that imidazole-derived H2-receptor antagonists (cimetidine and etintidine) and non-imidazole H2-receptor antagonists (famotidine, ranitidine and TZU-0460) compete with histamine at different sites on the H2-receptor of the gastric glands.View full abstractDownload PDF (501K) -
Atsuko SHINOHARA, Tetsuya KAMATAKI, Tetsutaro IIZUKA, Yuzuru ISHIMURA, ...1987 Volume 45 Issue 1 Pages 107-114
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSDrug oxidations by horseradish peroxidase (HRP), myoglobin (Mb) and cytochrome P-450cam (P-450cam) reconstituted with synthetic hemes were studied in comparison with a form of cytochrome P-450 purified from liver microsomes of polychlorinated biphenyl (PCB)-treated rats. N, N-Dimethylaniline (DMA) and 7-isopropoxycoumarin were hardly dealkylated by the heme-substituted proteins in the presence of NADPH-cytochrome c (P-450) reductase and NADPH, while substantial activity of this kind was observed in the presence of hydrogen peroxide or cumene hydroperoxide as oxygen donors. Specific activity varied, depending on the substrates, oxygen donors, heme derivatives and apoproteins employed. Very high levels of activity were observed in hydrogen peroxide-dependent DMA N-demethylation with HRP substituted with certain hemes. The highest level of activity was about two hundred times as high as that of rat liver cytochrome P-450. The relationship between such activity and the chemical structure of heme derivatives was discussed.View full abstractDownload PDF (385K) -
Takashi MATSUBARA, Shigemi OTSUBO, Ayako OGAWA, Hiroyuki NAKAO1987 Volume 45 Issue 1 Pages 115-119
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of several beta-lactam antibiotics on the acetaldehyde-metabolizing system were studied using germ-free rats. Administration of cefamandole (CMD) to the rats caused a decrease in liver mitochondrial low Km aldehyde dehydrogenase activity and an increase in blood acetaldehyde level during ethanol metabolism, similar to the case in conventional rats. Oral administration of CMD produced a pronounced increase in blood acetaldehyde level compared to the subcutaneous administration of the antibiotic. When the animals were given various beta-lactam antibiotics subcutaneously, only the antibiotics having an N-methyltetrazolylthiomethyl group at the 3-position of the cephalosporin nucleus exhibited the disulfiram-like effects on the acetaldehyde-metabolizing system. The results indicate that intestinal bacteria do no participate in the development of the disulfiram-like reaction of several beta-lactam antibiotics.View full abstractDownload PDF (263K) -
Isao KAMIYA, Toshiaki SUMITA, Naohisa ISHIKAWA1987 Volume 45 Issue 1 Pages 121-124
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSA canine lung-perfusion preparation was used to evaluate the role of serotonin receptor subtype in the development of serotonin-induced pulmonary edema. Ketanserin, an S2-receptor antagonist, blocked an increase in pulmonary arterial pressure caused by serotonin, but not the development of pulmonary edema. Methysergide, an S1- and S2-receptor antagonist, prevented the increase in pulmonary arterial pressure and edema formation caused by serotonin. These results suggest that the S1-receptor may participate in the development of pulmonary edema.View full abstractDownload PDF (231K) -
Sadaaki MAEDA, Junji NAKAMAE, Reizo INOKI1987 Volume 45 Issue 1 Pages 125-128
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effect of various opiate agonists on the contraction of isolated rat atrium was investigated. Ethylketocyclazocine (EKC) (30-100 μM) and dynorphin-A(1-13) (10-30 μM), which are κ-type agonists, caused positive inotropic effects on electrically stimulated left atrium in a dose-dependent manner. In addition, EKC decreased the frequency of spontaneous beating in the right atrium. Morphine (μ-type), [Met5] and [Leu5]-enkephalin (δ-type) did not affect both the developed tension and frequency of contractions. These results indicate that the positive inotropic action is specific for κ-type opiate agonists.View full abstractDownload PDF (167K)
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