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Volume 73, Issue 3
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Seigo FUJIMOTO1977 Volume 73 Issue 3 Pages 257-266
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSProduction, transport, storage and release of antidiuretic hormone (ADH) in the hypothalamo-neurohypophysial system were investigated. ADH produced by nerve cells in the paraventricular and supraoptic nuclei of the hypothalamus is present in a form bound to the speicfic protein neurophysin, in the neurosecretary granula. Electric and chemical stimulation of these nuclei results in evoked release of ADH in ionic association with neurophysin from the neural lobes. Acetylcholine, norepinephrine, histamine, angiotensin II, gammaaminobutyric acid and L-glutamic acid have been regarded as candidates of chemical transmitters for the release of ADH in the hypothalamus. Prostaglandin (PG) E2 may be another important compound for central regulation of water metabolism. The possibility that PGE2 may be the transmitter or a modulator in the nuclei has to be considered. Serotonin, dopamine and taurine, however, may not be involved in the ADH releasing mechanisms in the hypothalamus. It appears that norepinephrine, histamine, angiotensin II, PGE2 and bradykinin stimulate directly the neural lobe to release ADH. The ADH release is regulated by intracellular Ca++. The existence of a “readily-releasable pool” of ADH can be ruled out and any limitation in the amount of ADH released under experimental conditions may be due to insufficient activation of the neural lobe. A physiological significance other than a carrier was proposed for neurophysin.View full abstractDownload PDF (5380K) -
Tohru SHOJI, Keizo YONEKAWA, Takeshi TADANO, Kensuke KISARA1977 Volume 73 Issue 3 Pages 267-273
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSEffects of intracerebral (i.c.) administration of metaraminol (MA) on brain monoamine in mice were studied. The results were as follows: MA, dopamine (DA), noradrenaline (NA) and 5-hydroxytryptamine (5-HT) were separated with phosphate buffer using a phosphorylated cellulose column (1×11 cm, 9 ml, Lot No. 2809). When MA was i.c. injected into mice, native fluorescence of MA at 275/305 nm decreased in proportion to the time course and remained even at 12 hr after injection. Thirty min after MA in doses of either 40 or 80 μg, a significant decrease of DA as compared with that of saline-treated group occurred and MA in doses of 40, 80 and 160 μg produced a significant decrease of NA and 5-HT. Thirty min after 160 μg of MA, there was no significant difference in DA. Three hr after MA, DA levels significantly decreased, and 168 hr after were restored to the levels of the saline-treated group. Thirty min after MA, NA and 5-HT significantly decreased compared with those of the saline-treated group and recovery took place 48 hr and 168 hr after respectively. It was concluded that MA depletes not only NA but also DA and 5-HT in the mouse brain.View full abstractDownload PDF (3278K) -
Electron microscopic studies on the ultrastructural transformation of mitochondria in the cells of zona fasciculata of the adrenal cortex in morphine pellet implanted mice.Hiromi SENDA1977 Volume 73 Issue 3 Pages 275-286
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSInfluence of morphine on the fine structure of mitochondria in the cells of zona fasciculata of the adrenal cortex in mice in which a morphine pellet was subcutaneously implanted was studied using electron microscope. (1) Transformation of the mitochondrial structure, i.e. swelling, formation of lamellar or concentric circular cristae and decrease of electron density of the mitochondrial matrix, was observed 12 hr after implantation, and changes reached a maximum state at 48 hr. These transformations, however, disappeared within 4 days. (2) On the 4th day after implantation, removal of the pellet again produced transformation of the mitochondria with withdrawal symptoms, and a normal state was reverted to 72 hr later. Levallorphan challenge produced similar changes. (3) Injection of morphine into mice after removal of the pellet prevented the appearance of mitochondrial transformation. From the results obtained it may be concluded that there are correlations between the transformation of the mitochondria and physical dependence on morphine in mice.View full abstractDownload PDF (7895K) -
Kazuo HASEGAWA, Chieko ISHIBASHI1977 Volume 73 Issue 3 Pages 287-295
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSEffects of a new minor tranquilizer, CS-386, on the after-discharge(AD) and behavior induced by amygdaloid electrical stimulation in freely-moving cats were compared with those of cloxazolam, oxazolam, diazepam, chlordiazepoxide, phenobarbital and chlorpromazine. Effects on change of the AD threshold and duration and on facial twitching, salivation and tonic-clonic convulsion were investigated. CS-386, cloxazolam and oxazolam inhibited amygdaloid AD. CS-386 had the most potent inhibitory effect. These drugs depressed all behavior described above. Diazepam had no effects on the AD threshold, but decreased the AD duration and inhibited the behavior. Chlordiazepoxide had no apparent effects on amygdaloid AD and on facial twitching. Salivation was inhibited with high doses of administration. Phenobarbital shortened the AD duration and at a high dose elevated the AD threshold. This drug also inhibited salivation, but inhibitory effects on other behavior required doses as high as 90 mg/kg. These results suggest that CS-386, cloxazolam and oxazolam are compounds belonging to a classification different from that of chlorpromazine. CS-386 in particular, is a more potent drug than chlordiazepoxide, diazepam and phenobarbital and acts on the amygdala itself.View full abstractDownload PDF (4480K) -
Katsuya NAKAGAWA1977 Volume 73 Issue 3 Pages 297-305
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSMAO activity in rat brian mitochondria with tyramine as substrate at 100% oxygen concentration was three times as much as that at 20%. When serotonin served as substrate, difference in activities between the two oxygen concentrations was not significant. Similar results were obtained when rat liver MAO was used as the enzyme source. At 100% oxygen concentration, pargyline showed the most potent inhibition of MAO activity in liver mitochondria with tyramine as substrate, but inhibitions caused by pheniprazine and harmaline were not remarkable. At 100% oxygen concentration, harmaline showed the most potent inhibition of MAO activity in the liver when serotonin served as substrate, while inhibitions of the MAO activity by pargyline and pheniprazine were weak. At 20% oxygen concentration, harmaline showed the most potent inhibition of MAO activity in the brain when serotonin was used as substrate. These inhibitions were studied using Lineweaver-Burk plots. Pargyline revealed a noncompetitive inhibition to MAO activity in liver and brain with tyramine and serotonin as substrate, harmaline a competitive inhibition to MAO activity in liver and brain with tyramine as substrate, while noncompetitive inhibition to MAO activity in liver and brain was evident when serotonin was used as the substrate.View full abstractDownload PDF (3925K) -
Yoichiro HIGUCHI, Michiko FUKAMACHI1977 Volume 73 Issue 3 Pages 307-319
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSIt is well known that high concentrations of hydrogen sulfide (approximately 1500 ppm) are exceedingly toxic. However, few studies have been done on the response of the living body exposed to this substance at a sublethal concentration (under 500 ppm). We analyzed the effect of hydrogen sulfide at various concentrations (100 ?? 500 ppm) in Wistar strain rats which were well trained on conditioned avoidance response, and we found that discriminated avoidance response was significantly inhibited immediately after exposure to 200 ppm at the minimum, but significant inhibition of Sidman-type avoidance response was observed after exposure to 300 ppm. There was no correlation between the inhibitory intensity and the response rate on the behavioral baseline. The extinction of Sidman-type avoidance response was significantly accelerated only when the animal was exposed to a concentration over 500 ppm. In case of exposure to 300 ?? 500 ppm of hydrogen sulfide, both the discriminated and Sidman-type avoidance responses were inhibited at a rate and intensity which paralleled the concentrations. At one hour after forced ventilation, however, the initial response level was restored, but in case of exposure to higher concentrations, the inhibitory effect sometimes persisted until the next day. With other rats placed under almost the same conditions, blood pressure, respiration and heart rates were determined without anesthesia, following the exposure to 100 ?? 500 ppm of hydrogen sulfide. It was found that these values showed only transient deflections for about 5 min immediately after the exposure, but thereafter remained relatively stable for one hour. It was consequently assumed that inhibition of conditioned avoidance responses after exposure to hydorgen sulfide might be due to a depressive effect on the central nervous system.View full abstractDownload PDF (6182K) -
Yoshio SUZUKI, Yasuko HAMAGUCHI, Ichika YAMAGAMI1977 Volume 73 Issue 3 Pages 321-335
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSEffects of SE-1520 were compared with those of thiazide diuretics, hydrochlorothiazide (HCT) and trichlor-methiazide (TCM) in rats and dogs. SE-1520 in an oral dose of 0.1 ?? 10.0 mg/kg resulted in a strong and dose-dependent increase in urine volume as well as in the urinary excretion of Na+ and Cl-, while that of K+ significantly increased with an oral dose over 3.0 mg/kg. In experimental acidotic, alkalotic, nephritic and spontaneously hypertensive rats, almost the same strong natriuretic activity seen in normal rats was observed with SE-1520. The diuretic potency of these three diuretics in rats was MCT≥SE-1520>HCT. SE-1520 also exhibited a strong diuretic activity in dogs. In the renal clearance test of dogs, SE-1520 0.1 ?? 1.0 mg/kg i.v. did not influence the renal plasma flow (RPF) or glomerular filtration rate (GFR). The renal tubular Na+ reabsorption rate decreased by a maximum of 2.11% and the urinary Na+ excretion increased by 15.3 times the normal level 20 min after the injection of SE-1520 in a dose of 1.0 mg/kg i.v. From the results of clearance test and stop flow test in dogs, the site of action of SE-1520 was observed to be mainly in the distal tubules.View full abstractDownload PDF (6998K) -
Takeshi HONMA, Sumio KITAGAWA1977 Volume 73 Issue 3 Pages 337-345
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSMinor tranquilizers (diazepam, nitrazepam, oxazepam, bromazepam, medazepam, fludiazepam, meprobamate) at low doses increased ambulation score to 145 ?? 288% of control rats. Nitrazepam, diazepam and bromazepam which are potent, clinically prescribed minor tranquilizers increased the ambulation at lower doses than was seen with the other drugs. Fludiazepam and nitrazepam showed a maximum increase in ambulation at the same dose. Fludiazepam, nitrazepam and diazepam proved to have potent inhibitory effects on defecation. Trifluperidol, haloperidol and ID-4708 (a new butyrophenone derivative) and chlorpromazine when given at low doses reduced ambulation, while at higher doses defecation was inhibited. These four drugs reduced ambulation and elicited a recover in rates of defecation in methamphetaminetreated rats. Clozapine, thioridazine and floropipamide inhibited defecation at nearly the same doses which reduced ambulation in rats not given the methamphetamine treatment. These three drugs reduced ambulation, but did not produce a recovery in the defecation rates in methamphetamine-treated rats. These results indicate that neuroleptics such as clozapine which rarely induce extrapyramidal side-effects when clinically prescribed, inhibit defecation at nearly the same doses which reduce ambulation. In methamphetamine-treated rats, haloperidol was 31 times more potent than chlorpromazine in inhibiting activity noted with ambulation. This ratio in open-field test was close to the ratio of potency of these drugs as antipsychotic clinically prescribed agents.View full abstractDownload PDF (4001K) -
Michitada SASAJIMA, Hironaka AIHARA, Fusao AKIYAMA, Katsuharu TSUCHIDA ...1977 Volume 73 Issue 3 Pages 347-358
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSTolerance to chlorphenesin carbamate (CPC) was investigated from the viewpoints of action of CPC, serum free CPC concentration, the activity of UDP-glucuronyltransferase and the content of cytochrome P-450. CPC was administered once daily for 7 or 14 days. In mice, the hypnotic action of hexobarbital injected 24 hours after the last administration of CPC and the motor incoordinating action of CPC significantly decreased on the 7th day, but slightly recovered on the 14th day. Serum free CPC concentration also decreased on the 7th day, but recovered on the 14th day. A significant relationship between the motor incoordinating action of CPC and serum free CPC concentration was observed. Therefore, the recovery of CPC effect on the 14th day was considered to be due to the recovery from the induction of drug-metabolizing enzymes. On the other hand, in rats, the weekly alteration of the motor incoordinating action of CPC was similar to that observed in mice. Serum free CPC concentration on the 7th and 14th days was lower than that on the 1st day, and enzyme induction was observed during CPC administration. Notwithstanding the low level of serum free CPC concentration, the recovery of CPC effect was observed on the 14th day and such was considered to be due to habituation to the rotarod. In mice and rats, it was demonstrated that the intensity of CPC effect was dependent on serum free CPC concentration to the extent that enzyme induction played an important role in the development of tolerance. From these results, the tolerance to CPC is attributed to induction of drug-metabolizing enzymes in liver microsomes.View full abstractDownload PDF (4718K) -
Mitsuhiro Nagata, Atsuko Furumichi, Jun'o Shimamoto, Masao Morita1977 Volume 73 Issue 3 Pages 359-369
Published: 1977
Released on J-STAGE: March 29, 2007
JOURNAL FREE ACCESSThe effects of carteolol, propranolol and alprenolol were studied by using spontaneously contracting atria, atrial muscle and papillary muscle prepared from rat hearts. Propranolol, alprenolol and carteolol caused decreases in atrial rate and in contractile tension of electrically driven cardiac muscles in concentrations of 10-6 to 10-5 g/ml, 10-6 to 10-5 g/ml and 10-4 g/ml, respectively. These compounds, also, effectively prevented electrically-induced atrial arrhythmias in these concentrations. Contractile tension of the cardiac muscles was increased by carteolol in concentrations of 10-7 to 10-6 g/ml. The refractory period of the cardiac muscles was prolonged in the presence of alprenolol (10-7 to 10-6 g/ml) or carteolol (10-6 to 10-5 g/ml). The refractory period of the papillary muscle was increased by 10-7 to 10-6 g/ml of propranolol. The maximum driven frequency (MDF) of the atrial muscle was reduced by 5 × 10-8 to 10-7 g/ml of carteolol or by 5 × 10-8 g/ml of alprenolol, and MDF of the papillary muscle by 5 × 10-7 g/ml of propranolol. In extremely high concentrations, these compounds significantly reduced MDF of the cardiac muscles. These results suggest that the antiarrhythmic action of alprenolol and carteolol is more predominant in atria than in ventricles, whereas the reverse is true for propranolol.View full abstractDownload PDF (4689K)
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