Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 74, Issue 3
Displaying 1-11 of 11 articles from this issue
  • Akihide KODA, Kichiro INOUE, Kunihiro NAKAMURA, Hiroshi MORI
    1978 Volume 74 Issue 3 Pages 317-323
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Measurement of the excretion was carried out according to Sakuno's method with modifications, and the amount of protein and saccharide in the excretion was measured. The viscosity of excretion was also determined. With an i.p. injection of pilocarpine, a marked increase was observed in the amount of excretion and saccharide, and there was a slight decrease in the amount of protein. There was no appreciable change in viscosity. Such changes by pilocarpine in the excretion of airway were inhibited completely by a pretreatment with atropine. With noradrenaline there was a tendency for the amount of excretion and protein to decrease, and adrenaline caused no appreciable changes. A slight increase was observed in the viscosity after isoproterenol. With phentolamine, there was a slight decrease in the viscosity and protein, and a slight increase in the amount of saccharide. In contrast, propranolol clearly decreased the amount of excretion and saccharide. With a pretreatment of phentolamine, the amount of saccharide dramatically increased after noradrenaline, and the amount of excretion also increased after isoproterenol. On the other hand, with propranolol treatment, noradrenaline slightly decreased the amount of excretion, as well as protein and saccharide, and isoproterenol clearly decreased the amount of excretion with a slight decrease of protein. Continuous doses of isoproterenol for more than 2 weeks, dramatically increased the amount of excretion, protein and particulary the viscosity.
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  • Tadashige SHIMIZU, Yoshio AIZAWA
    1978 Volume 74 Issue 3 Pages 325-333
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Responsiveness of the rat uterus on the day of estrus to PGE2, PGFF and oxytocin was increased by administration of PGFi.p.24 hours prior to the experiments, but that of the uterus on the day of diestrus was not altered by the same treatment.The delayed action of PGF was not observed in the uterus of ovariectomized rats, but was observed in the uterus of estrogen treated rats. The delayed action of PGF was not evident in either the vas deferens or the intestine of the rat.
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  • Kiyoshi ARAKI, Tomiji OHASHI, Yasuo GOMI
    1978 Volume 74 Issue 3 Pages 335-343
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Effects of N, N-dimethylethylenediamines on epinephrine-induced pressor response in pentobarbital-anesthetized rats were examined and 3 out of 12 compounds, i.e., tripelennamine, N, N-dibenzyl-N', N'-dimethylethylenediamine (I) and N1, N1-dibenzyl-N2, N2-dimethyl-1, 2-propanediamine (II), were found to be more potent as potentiators to epinephrine. In pithed rats, tripelennamine, I, II and cocaine also augmented pressor response induced by epinephrine. In pentobarbital-anesthetized rats or in perfused hind paw of rats, the potentiation induced by cocaine and tripelennamine was more marked to norepinephrine than to epinephrine, but an inverse relation between norepinephrine and epinephrine was observed in the potentiation by I and II. In pentobarbital-anesthetized rats, tyramine-induced pressor responses were decreased or abolished by cocaine and tripelennamine, but these responses were increased by I and II. In pentobarbital-anesthetized rats, isoproterenol-, acetylcholine and histamine-induced depressor responses were not influenced by cocaine, tripelennamine, I and II. Sensitivity of reserpinized rats to epinephrine was increased about eight times that seen in pentobarbital-anesthetized rats. In reserpinized rats, epinephrine-induced pressor responses were slightly increased by cocaine, tripelennamine and II, but these potentiations were not dose-dependent. These results indicate that one of the sites of action of cocaine, tripelennamine, I and II is localized in the peripheral portion of cardiovascular system. The principal mode of action of cocaine and tripelennamine appears to be the inhibition of amine-uptake mechanism at sympathetic nerve endings. The mode of action of I and II is apparently different from the actions of cocaine and tripelennamine.
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  • Saizo YANAURA, Tomoo NISHIMURA, Tomokazu HOSOKAWA, Youichi ABE, Hiroak ...
    1978 Volume 74 Issue 3 Pages 345-352
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    To investigate the mechanism of the cough-like reflex (CLR), we employed 1. 1-dimethyl-4-phenylpiperazinium iodide (DMPP). In dogs anesthetized with α-chloralose, CLR was induced by administration of DMPP (i.v. and intracarotid arterial), lobeline and nicotine. Repeated administration of DMPP did not cause a tachphylaxis, however, lobeline and nicotine did induce a tachphylaxis. DMPP (i.a.), lobeline, nicotine and histamine caused an increase in respiratory resistance as measured by a Respiratory Resistance Meter, while DMPP (i.v.) did not. The ED50 of morphine, codeine, oxymethebanol, picoperidamine and piclobetol on CLR with DMPP was higher than that of those drugs employed for the peripherally-induced cough. CLR with DMPP was not affected by isoproterenol, ephedrine, atropine and propranolol. CLR was markedly depressed by hexarnethonium and slightly depressed by benzonatate. CLR was abolished after bilateral vagotomyor bilateral denervation of the carotid sinus nerves. These results indicate that the mechanism of CLR with DMPP is different from that of peripherally-induced cough and the carotid body chemoreceptor plays an important role in CLR with DMPP. This CLR may be useful for demonstrating the site of action and the mechanism of antitussive drugs.
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  • Hikaru OZAWA, Tsutomu MIURA, Masashi SATO
    1978 Volume 74 Issue 3 Pages 353-359
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Glycogen content and glycogen synthetase activity in mouse skeletal muscle (M. gastrocnemius) after single or repeated administrations of glucocorticoid were investigated and compared with those in liver, in a series of experiments to elucidate the biochemical mechanism of steroid myopathy. Results obtained were as follows. After a single administration of triamcinolone acetonide (TA, 5 mg/kg i.p.), glycogen content in muscle increased maximally at about 12 hr and returned to control level at about 24 hr. The I form activity of glycogen synthetase in muscle was increased only 6 hr after a single administration, while the total activity of the enzyme was not significantly changed. Similar results were obtained with the liver. After repeated administrations of TA for one week, the glycogen accumulation in the muscle was lowered markedly as compared with that after a single administration. No increase in synthetase I activity was observed, or rather, the enzyme activity was decreased as compared with that from control. Similar results were obtained with the liver. After single or repeated administrations, blood glucose level decreased slightly, glucose level of muscle was not affected and G-6-P level of muscle increased markedly. These results suggest that the lower accumulation of glycogen in the muscle after repeated administrations of glucocorticoid may be primarily due to an abnormality in the glycogen synthetase system.
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  • Hiroyuki KAWASHIMA, Kenji HOSHINA, Yoshiaki OKAMIYA, Tokutaro MAKITA, ...
    1978 Volume 74 Issue 3 Pages 361-382
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Effect of 1α-hydroxycholecalciferol on the metabolism of calcium and phosphorus was studied using Ca-labelled and non-labelled rats. With an oral daily dose of 2.5 or 12.5 μg/kg of 1α-hydroxycholecalciferol, serum calcium, urine volume, urinary calcium excretion, urinary calcium concentration and water consumption increased, while fecal concentration, urinary phosphorus concentration and food consumption decreased. There was a lag time (1 or 2 days) between the increase of serum calcium and that of specific activity of serum calcium, and bone resorption was stimulated later than was intestinal calcium transport. After 10 days treatment, calcium concentration in the femur decreased, while a remarkable calcification was noted in soft tissues such as kidney, intestine, aorta, heart and muscle, although these effects were reduced with lower doses of the drug. With a smaller oral daily dose (0.1 or 0.5 μg/kg), for 6 months, bone calcium and phosphorus concentration increased without soft tissue calcification. Thus, 1α-hydroxycholecalciferol may be an effective drug for patients with metabolic bone diseases.
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  • Hikaru OZAWA, Masayoshi GOTO, Michiko TAKAHASHI, Toshio UEMATSU
    1978 Volume 74 Issue 3 Pages 383-388
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    The influence of adrenergic agents, epinephrine and clonidine, on plasma immunoreactive insulin and plasma glucose concentrations was studied in mice. Subcutaneous injection of epinephrine in fasted mice did not alter the plasma glucose concentration (PG), while plasma immunoreactive insulin concentration (IRI) tended to increase gradually. Intravenous injection of glucose markedly increased IRI. Glucose-induced IRI increase was inhibited by a subcutaneous injection of epinephrine in spite of high elevation of PG. This inhibition of glucose-induced IRI increase by epinephrine was reversed after treatment with an α-adrenergic blocking agent, phentolamine. Propranolol, an β-adrenergic blocking agent suppressed IRI to a greater extent as compared with IRI induced by simultaneous injection of glucose and epinephrine. These results indicate that β-adrenoceptor stimulating action accelerates the insulin release induced by glucose while α-adrenoceptor stimulating action inhibits it. Subcutaneous injection of clonidine in fasted mice slightly decreased IRI and increased PG. The response of PG to clonidine was dose-dependent. Glucose-induced IRI increase was inhibited by an intravenous injection of clonidine, and PG was elevated under the same conditions. The inhibition of glucose-induced IRI increase by clonidine was reversed when phentolamine was given, and under these conditions, PG showed no change. Propranolol treatment did not result in a recovery of the inhibition of glucose-induced IRI increase by clonidine. When compared with the results of epinephrine treatment, it may be concluded that clonidine shows α-adrenoceptor stimulating action in the secretion of insulin from β-cells of the endocrine pancreas.
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  • Hachiro USUI, Mamoru KANDA, Seimei OSUMI, Takashi SEKI, Noboru TODA
    1978 Volume 74 Issue 3 Pages 389-396
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    The effect of indapamide, a high ceiling diuretic, antihypertensive drug, was investigated in helically-cut strips of rabbit cerebral, coronary, renal, mesensteric and femoral arteries and aortae. The addition of indapamide in concentrations higher than 3×10-5M relaxed those arterial strips contracted with prostaglandin F; the relaxation being greater in cerebral, coronary and renal arteries. Atropine, propranolol and aminophylline did not reduce the relaxing effect. Hydrochlorothiazide produced fewer incidences of relaxation. Treatment for 20 min with indapamide (3×10-5 or higher) significantly attenuated the contractile response of mesenteric arteries to nicotine and tyramine. Contractile responses to transmural electrical stimulation were not reduced but rather potentiated. The dose-response curve of norepinephrine was not significantly affected by indapamide. The contractile response of nictitating membranes of anesthetized cats to stimulation of preganglionic sympathetic nerves was not influenced by indapamide but was abolished by hexamethonium. It may be concluded that arterial relaxations induced by indapamide are due to a direct action on smooth muscles. Indapamide appears to attenuate the response to nicotine and tyramine by interfering with the mechanism of neuronal amine uptake. However, such does not involve a ganglionic blockade nor a reduction of the release of norepinephrine from adrenergic nerve terminals.
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  • Fujio ABE
    1978 Volume 74 Issue 3 Pages 397-407
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Effects of selective applications of drugs to the guinea pig hypogastric ganglion were studied on the contractile response of the vas deferens to the hypogastric nerve stimulation or to ganglionic stimulating drugs. Both acetylcholine (ACh) and dimethylphenylpiperazinium (DMPP) contracted the vas deferens. Neostigmine potentiated the ACh-induced contractions but not those which were DMPP-induced. Hemicholinium-3 (HC-3) reduced the response to nerve stimulation (R-NS) but affected neither the ACh-induced contractions nor the DMPP-induced contractions. Morphine blocked R-NS but not the ACh-induced and the DMPPinduced contractions. Hexamethonium reduced R-NS and the contractions to ACh or to DMPP. Methacholine and bethanechol applied before and after preganglionic tetanic stimulation of the hypogastric nerve produced no change of tone of the vas deferens. Atropine did not antagonize the responses which were produced by nerve stimulation, ACh or DMPP. These results support the classic hypothesis that ganglionic transmission is mediated by nicotinic receptors but do not provide evidence that muscarinic receptors exist at the synapses of this preparation.
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  • Fujio ABE, Takeshi OTORII
    1978 Volume 74 Issue 3 Pages 409-418
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Effect of sodium picrate (picric acid-Na; PA) on the hypogastric ganglion in the hypogastric nerve-vas deferens preparation of the guinea pig was studied and the results are as follows: PA or acetylcholine (ACh) at doses (g/ml) of 10-5 ?? 10-4 applied to the ganglion increased the height of the response (R-NS) of the vas deferens to the hypogastric nerve stimulation. Neither drug restored R-NS blocked by hexamethonium 3×10-5. Effects of PA and ACh on R-NS were potentiated by neostigmine 10-7 and the potentiation was considerably greater for ACh than for PA. Effects of PA on R-NS were not influenced by pretreatment with atropine. Both PA and ACh recovered R-NS which was partially reduced by hemicholinium-3 (HC-3), although the recovery of R-NS by PA was rapidly abolished more than that by ACh when these drugs were repeatedly applied in the presence of HC-3 3×10-5. PA markedly recovered the R-NS reduced by morphine 10-4 and ACh slightly restored that R-NS. These results suggest that the site of action of PA on the hypogastric ganglion of the guinea pig is different from that of ACh and the effect of PA on R-NS may be due to the acceleration of ACh-release from preganglionic nerve endings.
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  • Tsutomu KAMEYAMA, Toshitaka NABESHIMA, Kazuyuki TAKAHASHI
    1978 Volume 74 Issue 3 Pages 419-426
    Published: 1978
    Released on J-STAGE: March 29, 2007
    JOURNAL FREE ACCESS
    Determination of auditory threshold was carried out under a response duration schedule of tone and/or lightdipper presentation. This schedule enabled an exact assessment of auditory sensitivity, since the direction and distance from rat to sound source were constant and the rat could thus acquire the conditioned behavior in a short time. The rat has to press the lever and hold it until a CS(tone and/or light) was presented. The animal could get water-reinforcement with release of the lever during the period of CS. The intensity of 3 KHz pure tone was reduced, from 110 dB (starting point), by 2 dB steps in each trial, until the subject made 3 non-response trials(i.e., no dipper approach within 0.7 sec after the tone onset) among 5 trials. The highest tone intensity among non-response trials was taken as the threshold. The auditory sensitivity of the rats with cotton-stuffed ears and the pierced eardrums decreased about 10 and 20 dB, respectively. The auditory sensitivity in rats was decreased by administration of streptomycin sulfate(SM), 300 mg/kg/day, i.m., in combination with ethacrynic acid(EA), 50 mg/kg/day, p.o., for forty days and in combination with EA, 100 mg/ kg/day, p.o. for ten days. The auditory sensitivity was not influenced by administration of SM, 300 mg/kg/ day, i.m., for forty days.
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