All issues
Volume 79 (1982)
- Issue 6 Pages 461-
- Issue 5 Pages 343-
- Issue 4 Pages 237-
- Issue 3 Pages 113-
- Issue 2 Pages 77-
- Issue 1 Pages 1-
Volume 79, Issue 4
Displaying 1-10 of 10 articles from this issue
- |<
- <
- 1
- >
- >|
-
Haruhiko SHINOZAKI1982 Volume 79 Issue 4 Pages 237-249
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSThe actions of kainic acid, quisqualic acid, and ibotenic acid on the crayfish neuromuscular junction were described, and it was particularly interesting that the discrepancy between glutamate responses and EJPs was revealed by the use of kainic acid. On the other hand, there is increasing evidence showing that glutamate is an excitatory transmitter at the crayfish neuromuscular junction. At this stage, we are unable as yet to definitively support or reject glutamate's candidacy as the excitatory transmitter at the crayfish neuromuscular junction. The discrepancy revealed by the use of kainic acid may bring up some questions. Certainly, the differential action of kainic acid on the glutamate current and the excitatory synaptic current opens to doubt the transmitter role of glutamate. In the case of the study on a transmitter role for a substance of doubt status, the value of pharmacological studies seems to be greater in disproving than in asserting such the role. However, we have to consider the matter of the extra-junctional receptor postulated on the crayfish postsynaptic membrane as one of the major problems for pharmacological identification.View full abstractDownload PDF (6737K) -
Hiroshi MAEKAWA1982 Volume 79 Issue 4 Pages 251-261
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSSeveral investigators have confirmed that β-adrenoceptor blocking drugs produced a sustained pressor action in anesthetized rats. However, the mechanism of the pressor action has not been sufficiently explored. The following studies were done to further investigate the mechanism. (a) effects of pindolol, carteolol, propranolol, alprenolol, practolol and acebutolol (0.015 - 0.3 μmole/kg i.v.) on blood pressure of anesthetized rats, b) effects of these drugs on the positive chronotropic action and vasodilation induced by isoprenaline (0.1 μg/kg i.v.) in anesthetized rats, c) effects of these drugs on the increase in heart rate and contractile force of isolated rat and guinea pig atria induced by isoprenaline, d) effects of these drugs on the relaxation of isolated guinea pig trachea induced by isoprenaline. From these experiments, the magnitude of the pressor action of β-adrenoceptor blocking drugs in anesthetized rats was found to be more closely related to the magnitudes of inhibition produced by β-adrenoceptor blocking drugs on isoprenaline-induced relaxation of isolated guinea pig trachea and on isoprenaline-induced vasodilation in anesthetized rats than to those on isoprenaline-induced positive chronotropic and inotropic actions of isolated atria.View full abstractDownload PDF (4898K) -
Kazuhiro OHKUBO, Kenichi SUZUKI, Masaki OGUMA, Takeshi OTORII1982 Volume 79 Issue 4 Pages 263-274
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSThe effects of intracerebroventricular (i.c.v.) injection of guanfacine, a new antihypertensive agent, on blood pressure and heart rate were investigated and compared with those of clonidine in anaesthetized rabbits. The i.c.v. injection of guanfacine or clonidine induced a decrease in blood pressure and heart rate in doses which were ineffective by an intravenous route. The depressive effect of guanfacine was less than that of clonidine, but the duration of this action was obviously longer than that of clonidine. A fall in heart rate caused by guanfacine was always less conspicuous than that by clonidine in equipotent hypotensive doses. Decrease in blood pressure and heart rate caused by the two drugs were inhibited by i.c.v. pretreatment with phentolamine and 6-hydroxydopamine, respectively. These findings suggest that presynaptic and/or postsynaptic α-adrenoceptors in the brain may play an important role in the hypotension and bradycardia produced by guanfacine as well as clonidine. Furthermore, the uptake mechanism at the presynaptic sites of central noradrenergic neurons may be involved in the mode of hypotensive and bradycardic actions of these two drugs since these effects were abolished by pretreatment with desipramine, an inhibitor of noradrenaline uptake into the presynaptic nerve terminals.View full abstractDownload PDF (4216K) -
Ryuichiro ANDOH, Shinobu SAKURADA, Kensuke KISARA, Mitsuo TAKAHASHI, K ...1982 Volume 79 Issue 4 Pages 275-283
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSAlgesic actions of capsaicinoids were investigated by utilizing vocalization in conscious guinea pigs and medial thalamic neuronal activity in gallamine triethiodide immobilized cats. Intra-arterial administration of capsaicin and dihydrocapsaicin evoked strong vocalization response, but other capsaicinoids, nordihydrocapsaicin, homodihydrocapsaicin, homocapsaicin, norcapsaicin, N-(4-hydroxy-3-methoxybenzyl)-6-methylheptamide, and N-(4-hydroxy-3-methoxybenzyl)-6-methylhept-trans-4-enamide, were weaker than capsaicin and dihydrocapsaicin. Similar results were obtained from medial thalamic nociceptive neurons in cats. Morphine (10 mg/kg s.c.) suppressed vocalization response evoked by intra-arterial administration of capsaicin and bradykinin. Aspirin (100 mg/kg i.p.) also suppressed the bradykinin-evoked response, but not the capsaicin-evoked response. Capsi-amide, a non-pungent substance of Capsicum annuum L., failed to suppress nociceptive response to capsaicin or bradykinin in guinea pigs and cats. Tachyphylaxis was elicited by repeated administration of capsaicin in vocalization. No cross-tachyphylaxis to bradykinin, acetylcholine, and dihydrocapsaicin could be observed.View full abstractDownload PDF (3629K) -
Yohko IMAIZUMI, Minoru KATOH, Tatsuyoshi SUGIMOTO1982 Volume 79 Issue 4 Pages 285-291
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSThe effects of malotilate (diisopropyl 1, 3-dithiol-2-ylidenemalonate) on the synthesis and movement of RNA in rat liver were studied in order to elucidate the mechanism of protein synthesis induced by this drug. Incorporation of 3H-cytidine into various RNAs was followed to determine the rates of their synthesis. Oral administration of malotilate to rats enhanced the total RNA synthesis, which reached to maximum level 3 hr after administration. At that time, the increases in the incorporation of radioactivities into the total RNA and the nucleotide pool were closely related to the dosages. Malotilate significantly increased the polyribosomal and t-RNA synthesis as well as nuclear RNA, but not the movement of RNA from the nuclei to the cytosol. It is not likely that malotilate activates specific genes in chromatin because only about 0.1 nmole of malotilate and its metabolites per mg DNA was found in chromatin. From these results, a possible mechanism of protein synthesis induced by malotilate can be proposed as follows: malotilate primarily affects the post-transcription process, promoting the RNA synthesis in the nuclear fraction without any changes of DNA synthesis, and these consequent increases of the polyribosomal RNA and t-RNA synthesis result in the enhancement of protein synthesis.View full abstractDownload PDF (3208K) -
Hitoshi KATO1982 Volume 79 Issue 4 Pages 293-305
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSMorphological changes in rat sciatic nerve (SN) and plantar nerve (PN) induced by a thiamine deficient diet (TDD) and administration of oxythiamine (OT: 4 mg/ 100 g × 6 days) were observed, and thiamine (T) levels in rat nerve were simultaneously determined. Body weight gain ratio in rats which received OT fed a TDD (OTD group) was much reduced, and anorexia and ataxia were recognized in this group. Rats fed a regular diet, whose weights were restricted to be the same as those in the OTD group (EWC group), showed the symptoms of starvation. T levels of the SN and PN in the OT group, OTD group, and rats fed a TDD(TDD group) were reduced, but in the EWC group, T levels were the same as those in the control group (C group). There were myelin folds and myelin oboids in the EWC group, and these were recognized before axonal degeneration. In the TDD group, an increase in the number of mitochondria (Mit) was seen in the myelinated axon (MAx). In the OT and OTD groups, axonal degeneration (increase in the number of Mit, appearance of degenerated Mit, axonal shrinkage, and disappearance of neurofilament and neurotubule) was observed in the MAx. Degeneration of the MAx caused by TDD and OT was more severe in the PN than in the SN. Since these changes progressed from the peripheral nerve to the centripetal one, these changes in OTD group might be dying-back polyneuropathy.View full abstractDownload PDF (9498K) -
Masami SATO, Hisato KITAGAWA, Motohatsu FUJIWARA1982 Volume 79 Issue 4 Pages 307-315
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSThe effects of tofisopam on gastric functions were examined in rats. Intracerebroventricular (i.c.v.) injection of tofisopam (50 or 100 μg) increased both basal gastric acid output and mucosal blood flow (MBF) in rats anesthetized with urethane, while intravenous injection of tofisopam (10 mg/kg) did not change the basal gastric acid output. Ten μg of tofisopam, i.c.v., a dose which did not show any effect on the basal gastric acid output, significantly inhibited the decrease in gastric acid output induced by noradrenaline (5 μg, i.c.v.). Tofisopam (10 mg/kg, i.v. or 100 μg, i.c.v.) showed no effect on the increase in gastric acid output induced by electrical stimulation of the lateral hypothalamic area (LHA). These results, together with the previous findings, suggest that tofisopam (i.c.v.) acts on the nucleus dorsalis n. vagi and/or LHA and competes with noradrenaline. The gastric acid output was increased remarkably under water-immersion stress, and this increase lasted during the stress-loading, but the MBF did not show a corresponding increase. Pretreatment of rats with tofisopam (100 mg/kg, intraduodenal) significantly increased the MBF and inhibited the ulcer formation caused by the stress. From these results, tofisopam may restore the unbalance between sympathetic and parasympathetic nervous tones induced by stress-loading.View full abstractDownload PDF (3334K) -
Yoshio SUZUKI, Mikio ITO, Toshifumi KOMURA1982 Volume 79 Issue 4 Pages 317-325
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSEffects of azosemide on diuresis, plasma renin activity (PRA), and urinary prostaglandin E (PGE) excretion in normal rats and rats pretreated with indomethacin were studied in comparison with those of furosemide. Azosemide at doses ranging from 10 to 40 mg/kg p.o. dose-dependently increased urinary volume and Na+, K+, and Cl- excretions. In this case, the increases in urinary volume and Na+, K+, and Cl- excretions with 40 mg/kg of this drug were 3.4 and 4.1, 2.9, and 5.8 times, respectively. This drug at 30 mg/kg p.o. also increased the PRA and urinary PGE excretion by 3.8 and 2.9 times, respectively. Pretreatment with indomethacin (10 mg/kg × 3 p.o.), a PG synthesis inhibitor, inhibited the increasing effects of this drug on urinary volume and Na+ and Cl- excretions by 80 ?? 90%. Moreover, the increasing effects of this drug on PRA and urinary PGE excretion were also inhibited remarkably to the same degree by pretreatment with indomethacin. These effects of azosemide were roughly similar to those of furosemide. From these results, the diuretic action of azosemide, like that of furosemide, may partly be mediated through the activation of the PG system in kidney.View full abstractDownload PDF (3912K) -
Mikio ITO, Eiji YOKOCHI, Chikako KOBAYASHI, Yoshio SUZUKI1982 Volume 79 Issue 4 Pages 327-334
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSSevere ulcers were produced in rats by injections of 20% acetic acid in a volume of 0.05 ml into the subserosal layer of two portions in the corpus, and the effects of aceglutamide aluminum on hexosamine, sialic acid, uronic acid and hydroxyproline contents of the mucosa and stroma in the ulcerated regions were compared with the effects of L-glutamine. When aceglutamide aluminum (1, 000 mg/kg × 2/day) was orally administered for 4 consecutive days beginning the day of the operation, this drug inhibited the ulcer index and the perforations in ulcerated regions by 18 and 66%, respectively. In addition, the drug remarkably increased the total amounts (μg/ulcer areas/rat) of hexosamine, sialic acid, and uronic acid in the mucosa of ulcerated regions. It was notable that with the sialic acid contents, an increase in the concentration (μg/l00 mg dry tissue) was also observed. On the other hand, in the stroma of ulcerated regions, the contents of those components containing hydroxyproline were little affected by this drug. Following daily oral administration for 14 consecutive days, aceglutamide aluminum (1, 000 mg/kg × 2/day) brought about more potent effects than those following the 4 days administrations, and this drug showed a 37% inhibition of the ulcer index and a complete inhibition of the perforations. Moreover, the drug pronouncedly increased both total amounts and concentrations of hexosamine, sialic acid, and uronic acid in the mucosa in the ulcerated portions. Of these components, the increment of the sialic acid content was the greatest. In the stroma of ulcerated portions, total amounts and concentrations of those components containing hydroxyproline were significantly increased by this drug, although the increases in the stroma were less than those in the mucosa. These effects of aceglutamide aluminum were far more potent than those of L-glutamine at the same dose. From the above results, aceglutamide aluminum may accelerate ulcer repair by potentiating defensive factors through the increases of components forming the mucus and granuloma in ulcerated tissues.View full abstractDownload PDF (4059K) -
Taeko HATA, Tomitaro KITA, Akio NAMIMATSU, Eiji ITOH, Yasuo ODA1982 Volume 79 Issue 4 Pages 335-342
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSIn order to investigate the function of the circulatory system in SART rats, systolic blood pressure and regional arterial blood flow were examined. It was found in SART stressed rats that the blood pressure was about 10 mmHg lower than that of the non-stressed group on the 6th day of stressing and after stressing, and such low blood pressure was maintained for several days. SART rats showed a decrease in the average blood flow value in the common carotid artery, increases in the average and instantaneous maximum blood flow values in the superior mesenteric artery, and the instantaneous maximum blood flow value in the abdominal aorta had a tendency to increase, though little changes were observed in the renal and the femoral arteries. It was suggested by flow contours that there was hardening in the vessel walls of the common carotid artery and the abdominal aorta, and softening in the superior mesenteric artery. SART stress-induced hypotension was further decreased by a single dose of guanethidine, clonidine, or hydralazine, but not by neurotropin. Continuous preadministration of neurotropin prevented the SART stress-induced hypotension and changes in blood flow. From the above mentioned results, the sympathetic nerve may be thought to be decreased in tension, or be depressed, in the circulatory system of SART rats.View full abstractDownload PDF (4183K)
- |<
- <
- 1
- >
- >|