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S Hata

Publications and source records attributed to S Hata.

At least 217 records · Page 12Linked to original sources
PubMed1983

[Pharmacological investigation of rotational behaviors produced by unilateral electrical stimulation of the substantia nigra in the rat].

In order to elucidate pharmacological properties of rotational behaviour produced by unilateral electrical stimulation of the substantia nigra, effects of 6-hydroxydopamine treatment, dopamine receptor antagonists and agonists were investigated in the rat. Dopamine and its metabolites in the striatum were estimated after the stimulation. Intranigral treatment of 6-hydroxydopamine remarkably inhibited rotational behaviour induced by electrical stimulation. Antipsychotic drugs, 1 mg/kg haloperidol i.p. and 1 mg/kg pimozide i.p., decreased the behaviour by 50% of the control level. Sulpiride and metoclopramide did not exert significant influences on the behaviour. The dopamine receptor agonist apomorphine, 0.5 and 1 mg/kg s.c., markedly suppressed the stimulation-induced rotation, although it produced stereotypy, i.e. sniffing and gnawing. Bromocriptine, 10 mg/kg i.p., also suppressed rotational behaviour and produced locomotor activation without electrical stimulation. Methamphetamine did not have significant effects on the behaviour. Unilateral electrical stimulation of the substantia nigra produced an increase in the content of dopamine metabolites in the ipsilateral striatum of the rat pretreated with probenecid. These results suggest that the nigrostriatal dopaminergic system plays an important role in rotational behaviour produced by the electrical stimulation, and dopamine receptor agonists suppress the behaviour through a stimulating effect on the presynaptic dopamine receptor.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Antiteratogenic effects of tumor inhibitors, caffeine, antipain, and retinoic acid in mice.

To learn the effects of tumor inhibitors on chemically induced malformations, caffeine, antipain, and 13-trans-retinoic acid were given to pregnant ICR/Jcl mice after a single dose of urethan, N-hydroxyurethan, N-methyl-N-nitrosourea, N-ethyl-N-nitrosourea, or 4-nitroquinoline 1-oxide, which induces about 50% of the malformed fetuses. When caffeine was given immediately after carcinogen treatment on Day 10, urethan- and N-ethyl-N-nitrosourea-induced malformations were significantly suppressed by caffeine posttreatment, while N-hydroxyurethan- and N-methyl-N-nitrosourea-induced malformations were not suppressed by caffeine. 4-Nitroquinoline 1-oxide-initiated teratogenesis was also suppressed, but not significantly so (p not equal to 0.07). The results were very similar to those of the effects of caffeine on tumors induced by these carcinogens. Malformations of genetic origin (cleft palates and cleft lips) in CL/Fr mice were also suppressed significantly by caffeine treatment on Days 8 to 11, although the level of inhibition was less than that in chemically induced malformations. A protease inhibitor (antipromotor), antipain, also suppressed urethan-induced malformations. The antiteratogenic effects of antipain were most effective when it was given during the period of 24 to 48 hr after urethan treatment, while those of caffeine were most effective when it was given immediately after urethan. The promoting process might be involved in chemically induced teratogenesis, as it was in carcinogenesis. A natural retinoid (13-trans-retinoic acid) also suppressed urethan-induced malformations. Thus, tumors and malformations induced by chemical carcinogens were suppressed by tumor inhibitors, suggesting the similarity of both processes in the subcellular level, in spite of their morphological differences.

4-Nitroquinoline-1-oxide↗
PubMed1983

Effect of sucralfate on ethanol-induced gastric mucosal damage in the rat.

We studied the effect of sucralfate on ethanol-induced gastric mucosal damage in the rat. In doses of 25, 50, 100, 200, 400 and 800 mg/kg given 1.5 hr before the oral administration of 3 g/kg ethanol, sucralfate inhibited the development of erosions by 36, 62, 72, 90, 98 and 100 percent, respectively. Cimetidine, up to a dose of 160 mg/kg, was ineffective in this model. Sucralfate, in a dose of 400 mg/kg, also decreased the drop in transmucosal potential difference produced by the intragastric instillation of 3 ml of 20% ethanol from 21 mV to 13 mV. In separate experiments, pylorus-ligated rats received 125I-labeled human serum albumin intravenously and the leakage of 125I-radioactivity into the gastric lumen was studied as a parameter of mucosal permeability to macromolecules. Ethanol, in a dose of 3 g/kg, produced a two-fold increase in leakage over control. This was prevented by sucralfate (250 mg/kg) when given either 1.5 hr before or 3 hr after the dose of ethanol. The results of these experiments suggest that sucralfate protects the gastric mucosa against ethanol-induced damage by enhancing mucosal resistance.

Aluminum↗
PubMed1982

Effect of detergents on sterol synthesis in a cell-free system of yeast.

In order to obtain information about the reactivity of enzymes in sterol synthesis of yeast, the effects of some detergents were investigated. Among the detergents used, Triton X-100 was found to exert a unique action, and its effect on the incorporation of 14C-labeled acetate, mevalonate, farnesyl pyrophosphate, or S-adenosyl-L-methionine into squalene, 2,3-oxidosqualene, and sterols in a cell-free system was examined. Triton X-100 showed virtually no effect on the enzyme activities in the reactions from acetyl CoA to farnesyl pyrophosphate, but it had a marked effect on reactions from farnesyl pyrophosphate to ergosterol. Evidence was obtained suggesting that Triton X-100 apparently activated squalene synthetase (EC 2.5.1.21) but inhibited squalene epoxidase (EC 1.14.99.7) and delta 24-sterol methyltransferase (EC 2.1.1.41). The activity of epoxidase was protected from the inhibition by increasing the concentration of cell-free extracts or by the prior addition of lecithin liposomes to the reaction mixture. The inhibition of methyltransferase was partially reversed by treatment with Bio-heads SM-2, but that of epoxidase was not reversed by the treatment.

Cell Membrane↗
PubMed1982

Possible mechanisms of 15-hydroperoxyarachidonic acid-induced contraction of the canine basilar artery in vitro.

Pharmacological studies of the contraction induced by 15-hydroperoxyarachidonic acid (15-HPAA) were done in the isolated canine basilar artery. The maximal contractile force produced by 15-HPAA was 1.5 times that of serotonin and was equivalent to that of prostaglandin (PG) F2 alpha or PGA1. At concentrations in which reductions of [14C]-6-keto-PGF1 alpha (the breakdown product of PGI2) occurred, both 15-HPAA and tranylcypromine contracted the artery, whereas indomethacin consistently relaxed it. In the case of indomethacin, as the drug inhibited the synthesis of [14C]-PGE2, F2 alpha and thromboxane(TX) B2 (the breakdown product of TXA2) as well, it has been considered that the balances between PGI2 and other vasoconstrictive PGs or TX may regulate the tone of the artery. Furthermore, it was shown that 15-HPAA enhanced the synthesis of lipoxygenase products from [14C]arachidonic acid. Experiments were done, therefore, to know whether these enhanced lipoxygenase products participated in the manifestation of contraction induced by 15-HPAA or not. As a result, although indomethacin did not affect the contraction, significant reductions of the contraction were shown by eicosatetraynoic acid. These results suggest that enhanced synthesis of lipoxygenase products may be involved in eliciting contractile responses of 15-HPAA.

Animals↗
PubMed1981

Effect of sodium intake on angiotensin-converting enzyme activity of aorta in rats.

1. The effect of sodium intake on angiotensin-converting enzyme activity in subcellular fractions of aorta (homogenate, mitochondria, microsomes and supernatant) was studied in normotensive and spontaneously hypertensive rats. 2. Angiotensin-converting enzyme activity was extremely high in the supernatant fraction in normotensive and spontaneously hypertensive rats. 3. Total converting enzyme activity in spontaneously hypertensive rats was 34% higher than that in normotensive rats. 4. Increased sodium intake resulted in a marked reduction, almost to zero, of converting enzyme activity in each fraction of aorta in normotensive and spontaneously hypertensive rats. 5. Converting enzyme, widely distributed in subcellular fractions of the aorta, may play a possible rôle in the local control of vascular tone. It is likely that sodium intake inhibits production of the enzyme in vascular tissue.

Animals↗
PubMed1981

Subcellular localization of the enzymes involved in the late stage of ergosterol biosynthesis in yeast.

The subcellular distribution of enzymes involved in the reaction sequence from zymosterol to ergosterol was studied. The spheroplasts obtained from cells aerobically grown on ethanol were gently disrupted and the homogenate was fractionated into the subcellular organelles by differential centrifugation. Inspection of the distribution of several marker enzymes revealed that the fractionation was reasonably effected. As a result of experiments, delta 8-delta 7-sterol isomerase, S-adenosylmethionine: delta 24-sterol methyltransferase and the enzyme involved in the reaction sequence from episterol to ergosterol were localized in microsomes. These results suggest the localization of enzymes involved in the late stage of ergosterol synthesis in microsomes.

Cholestadienols↗
PubMed1981

Methacholine, a cholinergic agent, stimulates catecholamine release in man.

To study the effect of cholinergic stimulation on catecholamine release, methacholine, a choline ester, was injected im into normal subjects. Significant increases in plasma norepinephrine and plasma epinephrine concentrations were observed in response to methacholine administration with significant haemodynamic changes, but there was no correlation between the rise in plasma catecholamines and the haemodynamic changes. These results suggest that the increases in plasma catecholamines induced by methacholine did not result from reflex responses to haemodynamic changes and thus could be a direct effect of methacholine on sympathetic nerves and the adrenal medulla.

Adult↗