The Japanese Journal of Pharmacology
Online ISSN : 1347-3506
Print ISSN : 0021-5198
ISSN-L : 0021-5198
Volume 42, Issue 1
Displaying 1-19 of 19 articles from this issue
  • Yoshiyuki INADA, Masao TANABE, Yumiko SHIBOUTA, Katsuyoshi KAWAZOE, Ko ...
    1986 Volume 42 Issue 1 Pages 1-8
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    The antihypertensive action of N-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-N-(indan-2-yl)glycine hydrochloride (CV-3317), a nonsulfhydryl compound characterized as an angiotensin converting enzyme inhibitor in our previous work, was examined in hypertensive animal models. In 2-kidney, 1 clip hypertensive rats and dogs, CV-331 7 (3 and/or 10 mg/kg, p.o.) produced a sustained antihypertensive action of about 15 to 25 mmHg. Daily oral administrations of CV-3317 (1 to 10 mg/kg/day) to spontaneously hypertensive rats (SHR) for 5 weeks produced a sustained antihypertensive action of 20 to 40 mmHg. When CV-3317 (3 mg/kg) was combined with hydrochlorothiazide (10 mg/kg), its antihypertensive action was intensified in potency and duration. CV-3317 (30 mg/ kg) induced a slight hypotension (5 to 10 mmHg) in normotensive rats, but had no effect on the blood pressure of 1 -kidney, 1 clip hypertensive rats and on that of a low renin type of DOCA/salt hypertensive rat. The antihypertensive activity of CV-3317 was more potent than that of captopril. In pithed SHR, the pressor response induced by an electrical stimulation of the preganglionic sympathetic nerve, but not the pressor response to norepinephrine, was attenuated by both agents (0.3 mg/kg, i.v.). Both agents may exert their antihypertensive action not only primarily by inhibiting the renin-angiotensin system, but also by inhibiting norepinephrine release from the sympathetic nerve terminals indirectly by reducing the formation of vascular angiotensin II.
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  • Mitsuo KAWADA, Keisuke SATOH, Norio TAIRA
    1986 Volume 42 Issue 1 Pages 9-18
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    The cardiohemodynamic effects of nipradilol (K-351) were studied in comparison with those of propranolol, nadolol and prazosin in anesthetized, openchest dogs. All drugs were administered intravenously. Nipradilol produced dosedependent decreases in systemic blood pressure (BP), heart rate (HR), venous return (VR) and cardiac output (COP), but virtually no change in right atrial pressure (RAP). Propranolol decreased HR, tended to decrease VR and COP and increased RAP, but produced no change in systemic BP. Nadolol also decreased HR, VR and COP and increased RAP, but did not change systemic BP. Prazosin decreased systemic BP, VR and COP and tended to decrease RAP, but scarcely affected HR. After propranolol or nadolol, nipradilol failed to reduce HR, but still produced definite decreases in systemic BP, VR and COP and a slight decrease in RAP. After prazosin, nipradilol still produced decreases in systemic BP, HR, VR and COP. These results suggest that nipradilol decreases VR and COP mainly by increasing venous capacitance through direct venodilator action and in part by increasing resistance to VR through beta-adrenoceptor blockade. This effect also appears to be responsible for its hypotensive effect.
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  • Kyoichi KAGAWA, Hisako MATSUTAKA, Yukari YAMAGUCHI, Chizuko FUKUHAMA
    1986 Volume 42 Issue 1 Pages 19-26
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    Carbon tetrachloride (CCl4) enhances lipid peroxidation, resulting in triglyceride accumulation in the liver. In this report, we studied the therapeutic, but not the preventive, effect of garlic extract on CCl4-intoxicated liver, in comparison to the effect of vitamin E. Garlic extract was given orally to mice in the dose of 10, 100 or 500 mg/kg at 6 hr after CCl4 administration. The increased conjugateddiene level was diminished significantly to 82% by the 100 mg/kg extract, and also thiobarbituric acid-reactivity was inhibited by all the doses of the extract. In addition to the above mentioned effects, the high doses of garlic extract lowered hepatic triglyceride and lipid contents. Highly significant and positive correlation was observed between hepatic triglyceride content and conjugated-diene level in the lipid fraction of the liver. Besides, vitamin E at the dose of 25 mg/kg inhibited only lipid peroxidation. We, therefore, conclude that not only is garlic extract effective on diminution of lipid peroxide and on alteration of peroxidative status to more reductive condition like the effect of vitamin E, but it also inhibits hepatic triglyceride accumulation in injured liver.
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  • Chizuko KOSEKI, Yasushi KANAI, Yujiro HAYASHI, Norio OHNUMA, Masashi I ...
    1986 Volume 42 Issue 1 Pages 27-33
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    We examined intrarenal localization of receptors for α-rat atrial natriuretic polypeptide (α-rANP) by injecting [125I]-labeled ligand in vivo into the rat aorta. We found that the receptors for α-rANP are distributed also on the vasa recta of the outer and inner medulla in addition to the previously reported sites, i.e., the renal arteries, renal pelvis, glomeruli, and inner medullary tissues including collecting tubules. In the vascular bundle of the outer medulla, the majority of grains was preferentially localized on the arterial vasa recta. The electron microscopic autoradiography of the glomerulus showed that the binding sites were mainly localized on the foot process of the podocyte. Since α-rANP injected into the aorta under physiological conditions was bound to the glomerulus and vasa recta in the kidney, the effect of ANP on these binding sites may be important in the mechanism of natriuresis.
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  • Susumu YASUOKA, Yasuo NII, Fumitaka OHGUSHI, Kenji FUJISAWA, Tomohiro ...
    1986 Volume 42 Issue 1 Pages 35-41
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    The effects of N-(3, 4-dimethoxycinnamoyl)anthranilic acid (N-5') on the release of the slow-reacting substance (SRS) by zymosan or Ca ionophorestimulated rat and human alveolar macrophages (AM) were examined in vitro. Disodium cromoglycate (DSCG) was used as a control. N-5' at concentrations of 10-4-10-3 M significantly inhibited the release of SRS from both rat and human AM stimulated by zymosan. N-5' had almost the same inhibitory effect when added to the AM culture system at any time from 180 min before to 30 min after the addition of zymosan. N-5' (10-4-10-3 M) also significantly inhibited the release of SRS by Ca ionophore-stimulated rat AM. N-5' (10-6-10-3 M) had no significant effect on phagocytosis of yeast particles by rat AM. DSCG (10-6-10-3 M) did not inhibit the release of SRS from the zymosan-stimulated rat AM. N-5' was concluded to have a relatively specific inhibitory effect on the non-immunological release of SRS from stimulated AM. It is postulated that N-5' inhibits the process of release of SRS from AM by acting after the initial stage.
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  • Suying CUI, Midori KAJIWARA, Kaori ISHII, Kazuko AOKI, Junshi SAKAMOTO ...
    1986 Volume 42 Issue 1 Pages 43-49
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    The enkephalin-inactivating enzymes in rat vas deferens were studied by using the relatively specific inhibitor of each enzyme. The results showed that the rat vas deferens, like the other three preparations, guinea-pig ileum, mouse vas deferens and striatal membranes of guinea-pig brain, which had been investigated previously, contained three distinct enkephalin-hydrolyzing peptidases. Additionally, the enkephalin-hydrolyzing aminopeptidase, endopeptidase-24.11 and peptidyl dipeptidase A in rat vas deferens were found to be inhibited maximally with 1 μ of amastatin, 1 μM of phosphoramidon and 1 μM of captopril, respectively. In contrast to these three enzymes, both L-tyrosyl-L-tyrosine-sensitive dipeptidyl aminopeptidase and D-phenylalanine-sensitive carboxypeptidase were suggested not to be involved significantly in the inactivation of exogenously given enkephalin in rat vas deferens. The characteristics of the enkephalin-degradative enzymes in rat vas deferens were discussed in terms of their similarities to and differences from those in the other preparations.
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  • Reizo INOKI, Masafumi OKA, Sadaaki MAEDA, Katsuya IWATSUBO
    1986 Volume 42 Issue 1 Pages 51-61
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    Effects of conditioning stimulations of the nucleus raphe magnus (NRM), nucleus reticularis paragigantocellularis (NRPG), mesencephalic periaqueductal central gray (PAG), nucleus dorsomedialis hypothalami (DMH), corpus striatum (CP), sensory cortex (SCT) and visual cortex (VCT) and actions of morphine, naloxone and metergoline on the potentials recorded from the pars caudalis of the trigeminal sensory nucleus evoked by the electrical stimulation of rat incisor pulps were examined. 1) The spinal potentials evoked by electrical stimulation of the pulp consisted of 3 components. Component 2 was mainly inhibited by morphine and antagonized by naloxone. 2) Conditioning stimulation of NRM, NRPG, PAG, CP, SCT and DMH strongly inhibited component 2. VCT did not show any inhibition. 3) 33-67% of antagonism was observed by naloxone in the NRM, NRPG, PAG, CP, SCT and DMH. On the other hand, 27-44% of antagonism was observed by metergoline, and the antagonism was not enhanced by the additional administration of naloxone. These results conclusively show that the endorphin system as well as the serotonergic system is in the series involved in the descending inhibition for nociception in the trigeminal sensory nucleus.
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  • Atsushi MIYAMOTO, Toyoaki AKINO, Hideyo OHSHIKA
    1986 Volume 42 Issue 1 Pages 63-70
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    The effects of isoproterenol pretreatment on phosphatidylinositol turnover in rat parotid slices were studied to elucidate the relationship between β- and α1 -adrenoceptors. 32P-Labeling of phosphatidylinositol in parotid slices was increased by an α1- and α2-agonist (epinephrine and norepinephrine) and α1-agonists (methoxamine and phenylephrine), but not by an α2-agonist (clonidine) and a β-agonist (isoproterenol). Prazosin inhibited the increase in phosphatidylinositol turnover elicited by epinephrine, but propranolol did not. These results indicate that the stimulation of phosphatidylinositol turnover elicited by adrenergic agonists is mediated by activation of α1-adrenoceptors in the parotid glands. Isoproterenol pretreatment of the parotid slices caused a significant increase in 32P-labeling of phosphatidylinositol and a decrease in that of phosphatidic acid. The epinephrine or phenylephrine-induced increase in 32P-labeling of phosphatidylinositol were further enhanced by the isoproterenol pretreatment of the slices. In the isoproterenol-treated membranes of the parotid glands, [3H]prazosin binding to α1-receptors increased, but [3H]dihydroalprenolol binding to β-receptors did not. These findings indicate that the acceleration of phosphatidylinositol turnover induced by the isoproterenol pretreatment may be associated with an increase in α-adrenoceptor binding sites which might have appeared as a result of the isoproterenol pretreatment of the parotid slices.
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  • Seiichi SATO, Takashi KIM, Toshiaki ARAI, Shichiro MARUYAMA, Masamichi ...
    1986 Volume 42 Issue 1 Pages 71-78
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    The area of wound holes made in the parietal bone of 4-week-old rats was measured at 1, 2 and 4 weeks after the operation using Alizarin red S staining without the use of histological sections. Dexamethasone and indomethacin were administered s.c. after the operation every day except Sunday. The inhibitory action of dexamethasone on bone wound healing was stronger than that of indomethacin, as was its inhibitory action on skin wound healing. Inhibition of the age-related decrease in radiolucency of femurs and some changes in serum calcium level were also observed by dexamethasone administration, but not by indomethacin. These results suggest that dexamethasone inhibits bone wound healing through its effects on calcium metabolism in addition to its general inhibitory action on wound healing which is shared with indomethacin. Dexamethasone also strongly inhibited the decrease in Alcian blue stainability which occurs with an increase in age, both in the normal portion and in the wound hole portion of the calvaria, whereas indomethacin showed a weak inhibitory effect only in the wound hole portion. This result suggests that one of the mechanisms by which dexamethasone inhibits bone wound healing may be based on the retardation of mineralization caused by the inhibition of ramoval of acid mucopolysaccharide.
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  • Chiaki HARA, Nobuya OGAWA
    1986 Volume 42 Issue 1 Pages 79-85
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Several clinical papers have reported that beta-adrenoceptor antagonists were useful in the management of schizophrenia and tardive dyskinesia. The present study examined effects of beta-antagonists on haloperidol (HAL)-induced catalepsy using mice in order to study the relationship between beta-antagonists and central dopaminergic functions. Catalepsy was tested by the standard bar test 30 min after intraperitoneal treatment of HAL. Beta-antagonists were administered subcutaneously just after HAL-treatment. Propranolol, alprenolol, oxprenolol and pindolol increased the incidence of catalepsy compared to HAL alone. Atenolol, not penetrating into the brain, and the sedative and hypnotic drug chlord 1azepoxide did not potentiate it. These results suggest that the potentiation of HAL-catalepsy by beta-antagonists is based on their central action. Therefore, a central betareceptor appears to be implicated in the regulation of the central dopaminergic functions.
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  • Hideo YABANA, Kazuaki NAITO, Taku NAGAO
    1986 Volume 42 Issue 1 Pages 87-97
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Effects of chronic administration of denopamine on acute cardiovascular response to denopamine were studied in anesthetized rats. Effects of repeated treatment with isoproterenol was also investigated. The dose of denopamine to increase LV dp/dt max by 50% of the control (ED50) was 0.77 mg/kg, p.o. Following chronic administration of denopamine once daily at 10 or 20 mg/kg, p.o., for 14 days, the effect of denopamine (i.v.) on LV dp/dt max was similar to that in the control group. In the 40 mg/kg-group, however, the positive inotropic effect of denopamine (i.v.) was attenuated significantly at lower doses without a decrease in the maximal response and the ED50 was increased 1.8-fold. Chronic treatment with denopamine in the diet at 20 or 40 mg/kg/day for 14 days did not influence the response to the drug. By subcutaneous administration of 50 μg/kg isoproterenol, thrice daily for 3 days, the ED50 of isoproterenol (i.v.) for positive inotropy were increased 6.8-fold. In addition, the maximal response to isoproterenol was depressed to about 70% of that obtained in the control. In the preparation desensitized by isoproterenol (50 μg/kg), the inotropic response to denopamine was attenuated at lower doses, but the maximal response was not altered. In the groups desensitized by the two drugs, the positive chronotropic effect of the drugs (i.v.) tended to decrease and the effects on blood pressure was not changed. By Scatchard analysis, the specific 3H-dihydroalprenolol binding to the cardiac membranes (Bmax) was reduced in the 40 mg/kg denopamine (p.o.) group as well as in the isoproterenol-treated groups. In the 10 mg/kg denopamine and 20 mg/kg denopamine groups, however, Bmax was not changed. These results suggest that chronic administration of denopamine hardly results in desensitization of its positive inotropy at the effective doses.
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  • Yoshiyuki INADA, Zen-ichi TERASHITA, Yoshimi IMURA, Masao TANABE, Kohe ...
    1986 Volume 42 Issue 1 Pages 99-108
    Published: 1986
    Released on J-STAGE: September 15, 2006
    JOURNAL FREE ACCESS
    N-[N-[(S)-1-Ethoxycarbonyl-3-phenylpropyl]-L-alanyl]-N-(indan-2-yl)glycine hydrochloride (CV-3317) and its de-esterified products, CV-3317-COOH and CV-3317-(5-OH)-COOH, inhibited rabbit lung angiotensin converting enzyme (ACE) with the IC50s of 1.2×10-7, 4.0×10-8 and 4.0×10-8 M, respectively, angiotensin I(A-I)-induced vasoconstriction of the rat aorta (IC50: 2.6×10-7, 2.6×10-8 and 5.4×10-8 M, respectively), and A-I-induced pressor response of the rat kidney (IC50: 3.9×10-7, 3.5×10-8 and 2.8×10-8 M, respectively). In these 3 experiments, both de-esterified products were 4 to 14 times more potent than captopril. In rats, CV-3317 (0.0138 to 138 μmol/kg, p.o.) inhibited plasma and lung ACEs, and the effects at a dose of 0.46 μmol/kg lasted more than 8 hr. CV-331 7 inhibited the A-I-induced pressor action in rats (0.138 to 13.8 μmol/kg, p.o. or 0.046 to 0.138 μmol/kg, i.v.) and dogs (0.46 to 4.6 μmol/kg, p.o.) in a dose-related manner. CV-3317 was more potent and longer acting than captopril in these in vivo ACE inhibitions. CV-3317 augmented bradykinin-induced hypotension (dogs) and contraction of the ileum (guinea pigs) less potently than captopril. In spontaneously hypertensive rats (SH R), CV-3317 (3 mg/kg, p.o.) markedly inhibited plasma and tissue (aorta, kidney, lung and brain) ACEs; and when administered daily for 2 weeks, it inhibited the plasma, aorta, kidney and lung ACEs; in particular, it markedly inhibited the aortic ACE. Captopril (30 mg/kg, p.o.) markedly inhibited tissue ACEs and slightly plasma ACE, but its inhibitory effects on tissue ACEs, except for the aorta, were unclear by repeated closings and its effect on plasma ACE was rather enhanced. Thus, the inhibition of vascular ACE may be particularly important for the antihypertensive effect of the ACE inhibitors, includin CV-3317, in SHR.
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  • Tadashi NAGAMATSU, Yoshio SUZUKI
    1986 Volume 42 Issue 1 Pages 109-116
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Serum sickness nephritis was produced in rats by repeated i.v. injections of rabbit serum albumin. After 12 weeks of antigen injection, the rats with proteinuria were subjected to a renal biopsy. Then half of the group was continuously given 300 μg/rat/day of PGE1· α-cyclodextrin (PGE1·CD) with mini osmotic pumps for 3 weeks. PGE1·CD inhibited the development of glomerulonephritis and the deposition of immune complexes in the glomeruli, although the control group showed developed glomerular alteration and increased immune deposits in the glomeruli in the autopsy specimens. PGE1·CD particularly improved the intraluminal hypercellularity of the histological findings. In the early stage of this model, 0.5 and 1.0 mg/kg of PGE1 and 6.0, 12.5 and 25.0 mg/kg of azathioprine were administered s.c. and p.o., respectively, for 3 weeks. There was a significant suppression of about 20% in the 1.0 mg/kg PGE1 group on the antibody synthesis as compared with the control group throughout the experimental period, although the inhibition was less than that of azathioprine. In the same experimental protocol, PGE1 significantly suppressed the increase in leukocyte counts; at the third week after PGE1 the number of leukocytes was 25.6±4.2×103 in the control group and 14.1 ± 3.0×103 in the 1.0 mg/kg PGE1 group. It is considered that PGE1 could excert the antinephritic effect in this mode through decreasing the leukocyte counts in the circulation and the glomeruli independently of immune deposits in the glomeruli.
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  • Hidehiko NABATAME, Masashi SASA, Yukihiro OHNO, Shuji TAKAORI, Masakun ...
    1986 Volume 42 Issue 1 Pages 117-122
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Microiontophoretic studies were performed to elucidate the effects of phencyclidine (PCP) on neuronal activity in the lateral vestibular nucleus (LVN) of cats anesthetized with α-chloralose. Spikes elicited in the monosynaptic LVN neurons by vestibular nerve stimulation were not affected by iontophoretic application of PCP up to 100 nA, but they were blocked by atropine (30-50 nA). A dose-dependent increase in spontaneous firing during application of PCP was obtained in 11 of 15 monosynaptic neurons, in all of which firing was increased by iontophoretically applied acetylcholine (ACh). Simultaneous application of atropine completely inhibited the PCP and ACh-induced increase in the firing without affecting the glutamate-induced firing. These results indicate that PCP acts on the LVN monosynaptic neurons receiving input from the vestibular nerve in a similar manner to ACh.
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  • Susumu OKABE, Hiroki MIYAKE, Yumiko AWANE
    1986 Volume 42 Issue 1 Pages 123-133
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    NC-1300 (10-100 mg/kg), given p.o. at 0.5, 6, 12 or 24 hr before HCI·ethanol, dose-dependently protected the rat gastric mucosa. This protection was observed even when the gastric contents had been removed before application of HCl·ethanol. NC-1300 (30 mg/kg), given i.p., was without effect on lesion formation in a dose which potently inhibited gastric acid secretion in pylorusligated rats. Pretreatment with indomethacin (5 mg/kg, s.c.) resulted in no reduction in the protection by NC-1300, excluding the possible participation of endogenous prostaglandins in the protective mechanism. N-ethylmaleimide pretreatment (10 mg/kg, s.c.) slightly reduced the protective activity of NC-1300, suggesting the partial participation of endogenous sulfhydryl compounds in the NC-1300 protection. NC-1300 sulfide and mercaptobenzimidazole (compounds obtained after mixing NC-1300 with acidic solution) also dose-dependently protected against HCl·ethanol-induced lesions when given p.o. at 0.5 hr before HCl·ethanol. The protection was significant but was considerably reduced in contrast to NC-1300 when the compounds were given 12 hr beforehand. NC-1300 sulfone had no effect on lesion formation. Omeprazole (10, 30 mg/kg), given p.o., also dosedependently inhibited HCl-ethanol -induced lesions. However, the duration of protection was shorter than that seen with NC-1300, i.e., the effect disappeared 12 hr later. Thus, NC-1300 has a potent and long-lasting activity on HCl·ethanolinduced gastric lesions. The mechanism by which this occurs remains unknown.
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  • Hitoshi OHMORI, Toshihiko YAMAUCHI, Itaru YAMAMOTO
    1986 Volume 42 Issue 1 Pages 135-140
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Lipoic acid (Lip), a naturally occurring disulfide compound, was found to augment markedly in vitro antibody responses to sheep erythrocytes (SRBC), dinitrophenyl-Ficoll and trinitrophenyl-lipopolysaccharide (TNP-LPS) as effectively as 2-mercaptoethanol (2-ME) in murine lymphocytes. The mitogenic response to LPS or concanavalin A (Con A) was augmented by Lip only slightly. 2-ME has been reported to facilitate cystine utilization by the lymphocytes, but Lip did not, indicating that the mode of action of Lip is different from that of 2-ME. Lipaugmentation of anti-SRBC response was markedly abrogated when murine lymphocytes were depleted of T cells and cultured in the presence of Con A-conditioned medium containing T cell-replacing factor. The effect of Lip was also diminished in the response to TNP-LPS when the spleen cells were depleted of T cells. These observations suggest that Lip could augment the antibody response by stimulating a T cell subpopulation. This idea was confirmed by the experiment that Lip could enhance helper T cell activity which was induced by culturing murine lymphocytes with the antigen.
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  • Shigetoshi CHIBA, Miyoko TSUKADA
    1986 Volume 42 Issue 1 Pages 141-144
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Effects of angiotensin II on norepinephrine and KCl-induced vasoconstrictions were investigated in isolated canine mesenteric arteries which were perfused with Krebs' solution at 37°C. Angiotensin I I at 0.03-0.3 μg showed tachyphylaxis in the injection intervals used (10, 20 or 30 min intervals). After treatment with angiotensin II (0.18-1.8 μg), norepinephrine and KCl-induced constrictions were consistently potentiated. Imipramine which blocked tyramineinduced action did not significantly influence norepinephrine-induced constriction. Pretreatments with both angiotensin II and indomethacin enhanced norepinephrine-induced constriction much greater than that with angiotensin II alone. It is suggested that angiotensin II may modify intracellular Ca movements and prostaglandin production induced by norepinephrine.
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  • Yasuo TAKEDA, Yukio TAKANO, Hiro-o KAMIYA
    1986 Volume 42 Issue 1 Pages 145-149
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Intraperitoneal injection of cholecystokinin octapeptide (10 and 100 μg/kg, i.p.), but not the tetra-peptide (1 mg/kg, i.p.), into mice significantly reduced spontaneous locomotor activity in a dose-dependent manner. The increase in locomotor activity induced by methamphetamine (1 mg/kg, i.p.) and thyrotropin-releasing hormone (5 mg/kg, i.p.) was significantly reduced by cholecystokinin peptides. However, the inhibitory effects of these peptides differed. Neither the tetra nor octa peptide influenced the increased locomotor activity induced by nomifensine (5 mg/kg, i.p.), apomorphine (3 mg/kg, i.p.) or scopolamine (2 mg/kg, i.p.). Thus, these cholecystokinin peptides seem to selectively antagonize increased locomotor activity via the presynaptic dopaminergic system.
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  • Isamu OKUNO, Yumi FUJIHARU, Kiyohisa UCHIDA
    1986 Volume 42 Issue 1 Pages 150-152
    Published: 1986
    Released on J-STAGE: September 15, 2006
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    Latamoxef, cefamandole, carbenicillin and cefotaxime were examined for their effects on fibrinolytic activity in vitro by means of the fibrin plate method, fibrin clot lysis time and euglobulin lysis time with human, rabbit and rat plasma. These antibiotics showed no fibrinolytic but weak antifibrinolytic activity at 1000 or 3000 μg/ml in some assay systems.
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