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Volume 45 (1987)
- Issue 4 Pages 439-
- Issue 3 Pages 295-
- Issue 2 Pages 129-
- Issue 1 Pages 1-
Volume 45, Issue 2
Displaying 1-21 of 21 articles from this issue
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Yasunobu OKUMA, Kunihiko YOKOTANI, Yoshitsugu OSUMI1987 Volume 45 Issue 2 Pages 129-133
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSSites of inhibitory action of bombesin on gastric acid secretion were examined in rats anesthetized with urethane. Intracerebroventricular administration of bombesin (3-1000 pmole) dose-dependently inhibited the increase in gastric acid secretion induced by electrical stimulation of the vagus nerve (1 mA, 0.5 msec, 3 Hz). On the other hand, intrathecal (direct lumbar puncture) administration of bombesin, even in the large dose of 1 nmole, had no effect on the vagally stimulated gastric acid secretion. Three pmoles of bombesin microinjected into the preoptic area, the anterior hypothalamus and the paraventricular nucleus inhibited the vagus stimulated gastric acid secretion. Microinjection of this peptide into the ventromedial nucleus, the dorsomedial nucleus and the lateral hypothalamic area were without effect. A large electrolytic lesion of the anterior hypothalamus, including the preoptic-anterior hypothalamic area and the paraventricular nucleus, abolished the inhibitory effect of intracerebroventricularly applied bombesin, but a lesion re stricted to the preoptic-anterior hypothalamus or the paraventricular nucleus was without effect. We propose that the preoptic area, the anterior hypothalamus and the paraventricular nucleus are all involved in the inhibitory effect of bombesin on gastric acid secretion.View full abstractDownload PDF (290K) -
Toru EGASHIRA, Yasumitsu YAMANAKA1987 Volume 45 Issue 2 Pages 135-142
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSMale rats were given daily injections of 200 μg/kg I-thyroxine, s.c., for a period of 10 days. Monoamine oxidase (MAO) activities in the heart, lung and liver mitochondria decreased rapidly to about 50% those of the control rats with 5-HT and β-phenylethylamine (β-PEA) as substrates on the first day. After that, heart MAO activity increased gradually and exceeded the control value after 10 days with 5-HT as the substrate. The level of liver MAO activity was maintained at about 50-70% during the same period of administration with 5-HT as the substrate. The thyroxine treated rats showed no marked change in brain MAO activity. In vitro, I-thyroxine and its metabolites had no discriminative actions on MAO activities in these organs of rats. The heart, lung and liver MAO have unaltered Km values for 5-HT and β-PEA, but decreases in the Vmax for both substrates were observed between the control and I-thyroxine-treated rats. Addition of the brain, heart and liver cytosol fractions from I-thyroxine treated rats caused MAO activities of heart mitochondria to decrease with 5-HT as a substrate and caused them to increase with β-PEA as a substrate. MAO activities in liver also were inhibited by adding all the cytosols when β-PEA was the substrate, but on the contrary, lung MAO activities were increased when 5-HT was the substrate. These results indicate the possible presence of multiple modulators of MAO in the cytosol fractions of I-thyroxine treated rats.View full abstractDownload PDF (480K) -
Junko YOSHIDA, Shozo TAKAMURA, Shiro SUZUKI1987 Volume 45 Issue 2 Pages 143-147
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSAn antitumor acidic glycoprotein (SAG P) from Streptococcus pyogenes (Su strain) inhibited the growth of BALB/3T3 cells in culture in a dose-dependent manner (0.03-10.0 μg/ml). This effect of SAGP was abolished by washing the cells, suggesting that SAGP weakly binds to the cell membrane. The ability of the cells to form colonies was unaffected by three days exposure to SAGP. Cell cycle analysis by flow cytometry revealed an accumulation of SAGP-treated cells in the S-phase. SAGP (3 μg/ml) reduced the incorporation of 3H-thymidine into the cells to approximately half of the control level. These results suggest that SAGP inhibits the growth of target cells by acting on their surface membrane and decreasing the rate of DNA synthesis.View full abstractDownload PDF (271K) -
Yoshiki IWABUCHI, Chihiro AOKI, Taizo MASUHARA1987 Volume 45 Issue 2 Pages 149-158
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe action of dopamine (DA) on salivation and the secretion of marker glycoproteins (GP) from secretory cells of the rat submandibular gland (SMG) was investigated using various blockers at doses of 1 or 2 mg/kg (i.v.). DA at doses from 5 to 40 mg/kg (i.p.) dose-dependently increased salivation and the concentration of protein in SMG saliva. The order of inhibitory potency on salivation was propranolol (PPR)>phentolamine (PHN)>>haloperidol (HAL) when DA was administered i.p. at a dose of 10 mg/kg and PHN>>HAL>>PPR when the dose of DA was 40 mg/kg. The concentration of protein in saliva after pretreatment with HAL or PHN increased significantly at a dose of 40 mg/kg of DA, but did not increase at a dose of 10 mg/kg of DA. Moreover, pretreatment with PPR decreased it at both doses of DA. The electrophoretic profiles of GP in DA-evoked saliva showed two characteristic main bands of GP 1 (130 KDa) and GP IV (21.5 KDa) contained in the acinar cells (AC) and a minor band of GP III (31 KDa) which originated from the granular tubular cells (GT). The profile was not changed by pretreatment with PHN and HAL when DA was administered at a dose of 10 mg/kg, but at a dose of 40 mg/kg, the intensity of band I increased. Pretreatment with PPR, when DA was administered at 40 mg/kg, caused an increase in the intensity of band III and a reduction in that of band I. These results suggest that DA, at low doses, affects the AC, whereas at a higher dose, it affects both the AC and GT.View full abstractDownload PDF (501K) -
Naohisa ISHIKAWA, Itaru ICHIMURA, Motoshi KAINUMA, Tatsuro SHIGEI1987 Volume 45 Issue 2 Pages 159-167
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of isosorbide dinitrate (ISDN) on coronary flow and arterial prostaglandin (PG) concentrations were investigated, using dog heart-lung preparations. Two kinds of gases (low and high CO2 gases) were used for the arti-ficial respiration. Low CO2 gas contained 55% O2 and 0.2% CO2, whereas high CO2 gas contained 55% O2 and 8% CO2. Administration of ISDN into a blood reservoir at high CO2 caused an increase in coronary sinus blood flow, which was blocked by indomethacin, but not at low CO2. In the absence of ISDN, the arterial concentration of thromboxane (TX) B2 was larger at high CO2 than at low CO2. ISDN attenuated such an increase in TXB2 concentration caused by CO2. The arterial concentration of 6-keto PGF1α was altered by neither CO2 nor ISDN, but slightly increased with time. Indomethacin lowered the concentrations of 6-keto PGF1α and TXB2. These results suggested that the arterial CO2 tension enhanced the TXA2 synthesis and that ISDN inhibited such a relation between CO2 and TXA2 synthesis. Additionally, the vasodilatory effects of PGI2 was enhanced by elevating the arterial CO2 tension. Thus, the increase in canine coronary flow at high CO2 in the presence of ISDN may be related to the inhibitory effects of ISDN on the TXA2 synthesis enhanced by the high arterial CO2 tension and the facilitatory effects of CO2 on the PGI2-induced vasodilation.View full abstractDownload PDF (476K) -
Hirohiko SAKAMOTO, Nobuharu YOKOYAMA, Takashi NISHIMOTO, Kazuyuki MURA ...1987 Volume 45 Issue 2 Pages 169-175
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of a new tricyclic antidepressant drug, quinupramine, on the monoamine uptake of rat brain homogenate preparations were studied in comparison with imipramine. Pharmacokinetic studies on quinupramine and imipramine in plasma and brain were also performed in rats after a single oral administration. Quinupramine had few effects on the noradrenaline and serotonin uptake both in in vitro and ex vivo models. After the administration of [3H]quinupramine, the unchanged drug was estimated as 60-75% of the total radioactivity in the cerebral cortex. Imipramine and desipramine preferentially inhibited the uptake of serotonin and noradrenaline, respectively, in vitro. After the administration, imipramine showed a marked inhibitory effect on noradrenaline uptake. A considerable amount of desipramine but not imipramine could be detected in the brain and plasma after the adminisration of [3H]imipramine. These results demonstrate that 1) the anti-depressant activity of quinupramine cannot be attributed to inhibition of monoamine uptake, 2) unchanged quinupramine penetrates into the CNS and affects some of the processes of neurotransmission and 3) the pharmacological activities of imipramine, when administered orally, may be attributed to desipramine, the metabolite formed.View full abstractDownload PDF (399K) -
Yoshio SUZUKI, Yoshihito TSUKUSHI, Mikio ITO, Tadashi NAGAMATSU1987 Volume 45 Issue 2 Pages 177-185
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn order to investigate the antinephritic effect of Y-19018, a thromboxane A synthetase inhibitor, on crescentic-type anti-glomerular basement membrane (anti-GBM) nephritis in rats, the present study was undertaken. Male Sprague Dawley rats were immunized with rabbit γ-globulin in Freund's complete adjuvant following i.v. injection of anti-GBM serum. Y-19018 at a dose of 0.3 and 3.0 mg/kg was given orally to rats from the day after the injection of anti-GBM serum (day 1) to day 39. Y-19018, 3.0 mg/kg, significantly inhibited both urinary protein excretion (30.6%) on day 19 and plasma cholesterol (39.8%) on day 15. Moreover, light microscopy demonstrated that this drug at both doses remarkably prevented histological involvement of the glomeruli on day 40 in a dose-dependent manner. In the blood obtained from nephritic rats, platelet aggregation was increased. Y-19018 suppressed (48.7%) the hyperaggregability of platelets on day 40 at a high dose, although the suppression of platelet aggregation was not in a dose-dependent manner. It is concluded from these data that Y-19018 shows beneficial effects on crescentic-type anti-GBM nephritis and may exert its action partly through inhibition of glomerular TXA2.View full abstractDownload PDF (536K) -
Seiji ICHIDA, Shunji ARIYOSHI, Toshihiko TANAKA, Kenji SOBUE, Yuko OKA ...1987 Volume 45 Issue 2 Pages 187-195
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe characteristics of superprecipitation of uterine myosin B from 17β-estradiol-3-benzoate-treated rats and the effects of L-methionine and/or 3-deazaadenosine (3-DAA) plus homocysteine thiolactone (HCTL) on the reaction were investigated. The slope and plateau phases of the superprecipitation were dependent on ATP, calcium and magnesium. The calmodulin antagonists, trifluoperazine and N-(6-aminohexyl)-5-chloro-1-naphthalene sulfonamide, inhibited the slope and plateau phases, but not the basal superprecipitation. SDS-polyacrylamide gel electrophoresis of the precipitate obtained in complete medium showed the presence of actin and myosin. Addition of 3 mM L-methionine had little affect on either the slope or plateau phases of the basal or calcium-dependent superprecipitation, while 500 μM 3-DAA plus 1 mM HCTL caused only 9 to 20% decrease in the calcium-dependent superprecipitation in the presence of 0.1 mM or 1 mM ATP. These findings suggest that the calcium-dependent superprecipitation of rat uterine myosin B reflected the contractile response of uterine muscle, and that L-methionine and/or 3-DAA plus HCTL did not affect the calcium-dependent superprecipitation of uterine myosin B.View full abstractDownload PDF (480K) -
Ayako SUDO1987 Volume 45 Issue 2 Pages 197-201
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSAdrenaline is known to increase in extra-adrenal peripheral organs as well as urine and plasma in the rat after swimming stress. In order to clarify the physiological significance of adrenaline in stress responses, the origin and location of adrenaline in the peripheral organs were examined by measuring adrenaline in the heart, spleen, submaxillary gland and some other organs after adrenalectomy or guanethidine treatment. After bilateral adrenalectomy, adrenaline in the peripheral organs mostly disappeared. Swimming stress caused no increase in the adrenaline content of the organs in the adrenalectomized rats, while a marked increase was observed in the sham-operated animals. In guanethidine-treated rats, the adrenaline content of the peripheral organs was extremely low as compared to that in the saline-treated animals, and the swimming-induced increase in adrenaline level in the organs was greatly suppressed. These observations suggest that the organ adrenaline, which exists in sympathetic nerve endings, is mostly derived from the adrenal gland. It is considered that adrenaline would be involved in sympathetic neurotransmission, especially under stressful conditions.View full abstractDownload PDF (316K) -
Makoto TANAKA, Makoto MURAMATSU, Hironaka AIHARA1987 Volume 45 Issue 2 Pages 203-210
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSCD-349 (2-nitratopropyl 3-nitratopropyl 2, 6-dimethyl-4-(3-nitrophenyl)-1, 4-dihydropyridine-3, 5-dicarboxylate) inhibited the activity of cyclic AMP phosphodiesterase (PDE) from the porcine coronary artery more effectively than that from the myocardium. Other dihydropyridines, nicardipine and nifedipine, were not tissue selective in inhibiting the cyclic AMP PDE from both sources. CD-349 inhibited cyclic AMP PDE noncompetitively with apparent inhibition constant (Ki) values of 6.6 and 4.6 μM for high and low affinity constant (Km) enzymes, respectively. Basal activity of coronary arterial cyclic AMP PDE was decreased to approximately 65% of the control value by 0.2 mM ethylene glycol bis (β-aminoethyl ether)N, N, N', N'-tetraacetic acid (EGTA). In the coronary artery, the inhibition of cyclic AMP PDE by CD-349 was weakened in the presence of EGTA, while the inhibition of nicardipine and nifedipine were not affected. EGTA had no influence on the CD-349 induced inhibition of myocardial cyclic AMP PDE. Calmodulin antagonists such as trifluoperazine (TFP) gave substantially the same results as those with CD-349. These results indicate the relative selectivity of the coronary arterial cyclic AMP PDE inhibition by CD-349 and suggest that this selective inhibition is due to blockade of calcium/calmodulin-activated cyclic AMP PDE.View full abstractDownload PDF (409K) -
Nagao SUZUKI, Yasuo GOMI1987 Volume 45 Issue 2 Pages 211-221
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSContractile responses of the circular smooth muscle of the guinea-pig vas deferens to electrical stimulation were recorded isometrically using ring preparations of about 2 mm in breadth. Stimulation of low frequency (2.5 to 10 Hz, 0.05 msec duration) for 20 sec produced twitch contractions which occurred once or repetitively during the application of stimulation. Higher frequency stimulation (20 to 80 Hz) produced biphasic contractions, an initial phasic and a secondary tonic contraction. These contractions were abolished by 3×10-6M tetrodotoxin or 3×10-5M guanethidine; however, 3×10-6M atropine or hexamethonium did not affect the contractions. Prazosin at 10-6M, like 3×10-7M yohimbine, increased the amplitudes of twitch contractions to the low frequency stimulation and caused the twitch contractions to occur repetitively. On the other hand, prazosin suppressed the tonic contractions to the high frequency stimulation without substantially inhibiting the phasic contractions. Cocaine at 3×10-6M potentiated the twitch contractions in the presence of yohimbine. After in vivo reserpine treatments, the low and high frequency stimulation produced twitch and phasic contractions, respectively; however, tonic contractions were not induced. Prazosin at 10-6M did not qualitatively affect the contractions in preparations from the reserpine-treated animals. These results suggest that the neurogenic contractions of the circular muscle of the guinea-pig vas deferens are sympathetic in nature, but that they are not mediated solely by norepinephrine. Co-release of other transmitters was indicated to occur upon the electrical stimulation of wide frequency range.View full abstractDownload PDF (567K) -
Takashi MATSUBARA, Shigemi OTSUBO, Ayako OGAWA, Tatsushi OKA1987 Volume 45 Issue 2 Pages 223-232
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe disulfiram-like effect of beta-lactam antibiotics, having an N-methyltetrazolethiol (NMTT) as a 3'-position substituent of the cephalosporin nucleus, was determined in rats using latamoxef (LMOX) as a model. Intravenous and subcutaneous administrations of these antibiotics caused a decrease in the low Km aldehyde dehydrogenase (ALDH) activity in liver mitochondria and an increase in blood acetaldehyde level during ethanol metabolism, as in the case of disulfiram. When the antibiotic was administered intravenously to biliary fistula rats, the blood acetaldehyde level did not increase. On the other hand, oral administration of antibiotic to normal and biliary fistula rats caused pronounced development of disulfiram-like effects in both animals. When LMOX was injected to normal rats, the rapid and slow eliminations of LMOX and NMTT, respectively, were observed from blood and liver. After oral administration of LMOX, NMTT remained in the blood and liver for a long time with higher concentrations, although LMOX could not be detected in the body. With biliary fistula rats, intravenous injection of LMOX led to rapid urinary excretion of both LMOX and NMTT. These results indicate that the development of disulfiram-like effects of NMTT-containing antibiotics is closely related to the pharmacokinetic profile of NMTT released from its parent drugs.View full abstractDownload PDF (551K) -
Masahiro TOHKIN, Takashi MATSUBARA1987 Volume 45 Issue 2 Pages 233-242
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of adrenergic agonists and antagonists on hepatic glycogenolysis were investigated using isolated perfused rat liver. Comparative studies on the glucose output by various adrenergic agonists and the inhibitory action of various antagonists on epinephrine-induced glycogenolysis indicated that this glycogenolysis was mediated by α1-adrenergic receptors. Epinephrine-induced glucose output from the liver was detected repetitively when epinephrine was repeatedly added to the perfused liver, while the glucose output decreased gradually when epinephrine was infused repetitively to the liver perfused with Ca2+-free buffer. Infusion of epinephrine to the perfused liver caused a release of Ca2+ associated with the glucose output, and a close correlation was found between the amounts of glucose and Ca2+ released from the liver with the infusion of epinephrine at various concentrations. The amounts of glucose production induced by epinephrine in the absence of extracellular Ca2+ were smaller than in the presence of extracellular Ca2+ when the liver received a large or sustained stimulation of epinephrine. These results suggest that the epinephrine mobilizes Ca2+ from the intracellular store to activate glycogenolysis, while entry of extracellular Ca2+ into the cell is required in order to obtain a large or sustained hormonal stimulation of glycogenolysis and to supply the intracellular Ca2+ store.View full abstractDownload PDF (544K) -
Koji OKAMURA, Futoshi MATSUBARA, Yasuyuki YOSHIOKA, Noriaki KIKUCHI, Y ...1987 Volume 45 Issue 2 Pages 243-248
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSCentral fatigue was induced by running rats on a treadmill. Amino acid and ammonia metabolism in the brain and blood were followed with time to correlate its changes with physical exhaustion. The blood ammonia level did not change during running, but was prominently increased at exhaustion. The brain level of ammonia was also prominently high at the end of exercise with a time course of change similar to that of the blood level. Plasma concentrations of branched chain amino acids (BCAA) and aromatic amino acids (AAA) increased as the animals continued to run; however, the plasma BCAA/AAA ratio was definitely depressed at exhaustion. This was also true with the brain BCAA/AAA ratio. A positive correlation was demonstrated between the plasma and brain BCAA/AAA ratios at r=0.5040 and P<0.05. These exercise-related changes suggest that physical exercise-induced central fatigue involves not only an increase in brain am monia, but also a disturbance in brain amine metabolism accompanying plasma and brain BCAA/AAA ratio depression. Furthermore, the ammonia level and BCAA/ AAA ratio in the brain correlated with those in the blood. It is reasonable to consider that the blood ammonia concentration and plasma BCAA/AAA ratio may serve as important indices of the clinical condition of exercise-induced central fatigue.View full abstractDownload PDF (322K) -
Kazuho ABE, Norio MATSUKI, Yutaka KASUYA1987 Volume 45 Issue 2 Pages 249-261
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSPharmacological and electrophysiological properties of postsynaptic α-adrenoceptor subtypes in rat tail artery were compared using selective α1 and α2-adrenoceptor agonists. Five α-adrenoceptor agonists contracted the tail artery with the following order of maximal effects: norepinephrine (α1 and α2)>methoxamine (α1)=phenylephrine (α1)>>clonidine (α2)>UK-14, 304 (α2). Phenoxybenzamine greatly diminished contractions induced by methoxamine and phenylephrine, but had little effect on responses to UK-14, 304. Idazoxan antagonized more potently against UK-14, 304 than against methoxamine. These results suggest the heterogeneity of postsynaptic α-adrenoceptors in the rat tail artery. Furthermore, responses to methoxamine and phenylephrine 1) had faster onsets and 2) were more resistant to Ca2+ entry blockers, nicardipine and diltiazem, and a promotor, Bay K 8644, or decreasing of extracellular Ca2+ and 3) were more sensitive to a calmodulin antagonist, W-7, than the responses to UK-14, 304 and clonidine. Both methoxamine and UK-14, 304 depolarized the membrane but methoxamine produced stronger depolarization than UK-14, 304. Therefore, the high sensitivity of α2-adrenoceptor agonists-induced responses to Ca2+ entry blockers and promotors cannot be accounted for solely by membrane depolarization. These results may indicate the differences in the Ca2+ movement for the contractions produced by α1- and α2-adrenoceptor agonists.View full abstractDownload PDF (716K) -
Hidefumi NISHIKAWA, Kunihiko YOKOTANI, Motohatsu FUJIWARA1987 Volume 45 Issue 2 Pages 263-270
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of somatostatin on parasympathetically induced increases in gastric acid secretion and mucosal blood tlow (MBF) were studied in anesthetized rats with a gastric fistula. Intravenous infusion of small doses of somatostatin (0.1-0.5 μg/kg/min) dose-dependently inhibited the increases in the vagally stimulated gastric acid secretion. Larger doses of somatostatin (0.5-2.5 μg/kg/ min) also dose-dependently inhibited the bethanechol-induced gastric acid secretion. The dose of somatostatin required to inhibit the gastric acid secretion by about 50% of the preinfused control values was 0.25 μg/kg/min for vagally stimulated acid secretion and 2.5 μg/kg/min for bethanechol-induced acid secretion. Thus, the inhibitory potency of somatostatin on the vagally stimulated gastric acid secretion was about 10-fold higher than that on bethanechol-induced acid secretion. Somatostatin had no effect on the increase in gastric MBF during vagus nerve stimulation or bethanechol infusion. Pretreatment with indomethacin or phentolamine had no effect on the inhibitory effect of somatostatin on the increase in gastric acid secretion during vagus nerve stimulation or bethanechol infusion. These results suggest that somatostatin exerts an inhibitory effect on gastric acid secretion by acting on the parasympathetic neurons in the gastric wall more than on the structures peripheral to the parasympathetic nerve terminals, and it reduces parasympathetically stimulated gastric acid secretion in rats. This inhibitoty effect of somatostatin on the gastric acid secretion is independent of the changes in the gastric MBF and probably not related to prostaglandin-involved or alpha adrenoceptor-mediated mechanisms.View full abstractDownload PDF (502K) -
Yoshihiro SUZUKI, Jun-ichi SUDO1987 Volume 45 Issue 2 Pages 271-279
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn order to elucidate toxic and protective mechanisms responsible for allopurinol-induced nephrotoxicity in rats, we investigated changes in plasma creatinine concentration, renal lipid peroxidation, and renal activities of xanthine oxidase, superoxide dismutase and catalase, as enzymatic factors in producing and scavenging oxygn radicals. The rats received subcutaneous injections of allopurinol in a dose of 100 mg/kg body weight, once a day for 3 days. In comparison to the control rats, the following changes were observed in the allopurinol-administered rats: an increase in plasma creatinine concentration, increases in renal contents of malonaldehyde, hypoxanthine and xanthine, and an increase of renal activity of xanthine oxidase, and decreases in renal activities of superoxide dismutase and catalase. Peaks in these changes were observed coincidentally on the third day after the administration of the drug was started. Afterwards, these parameters all returned to the control levels. These results strongly suggested that the allopurinol nephrotoxicity was attributed to the increase of lipid peroxidation which had been caused both by an increase in the ability of producing the oxygen radicals and by a decrease in the ability of scavenging the radicals.View full abstractDownload PDF (511K) -
Junji MIYAKOSHI, Mitsuru HIRATA, Wasako ODA, Edward J. CRAGOE, Jr., Ch ...1987 Volume 45 Issue 2 Pages 281-283
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of five amiloride analogues on thermal cell killing were examined using Chinese hamster V-79 cells. When cells were exposed to 42°C hyperthermia in the presence of 0.2 mM amiloride or its analogue, cell survival decreased with increasing exposure time, as compared with that for exposure to 42°C alone. The degree of the thermosensitizing effect varied among the test compounds, and three analogues were found to be more potent than amiloride. The results suggest that some of the amiloride analogues may be useful as hyperthermic sensitizers in the clinical treatment of cancer.View full abstractDownload PDF (161K) -
Yohkazu MATSUSHIMA, Satoshi AKABANE, Minoru KAWAMURA, Keiichi ITO1987 Volume 45 Issue 2 Pages 284-287
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTo examine the localization of α-adrenoceptors within the kidney tubule, binding experiments with 125I-HEAT and 3H-yohimbine were performed using cortical homogenates, basoalteral membranes (BLM) and brush border membranes (BBM). Bmax values for 125I-HEAT or 3H-yohimbine binding were 2.3 or 2.0-fold that of the homogenate in BBM and 8.2- or 10.7-fold in BLM, respectively. Kd values for 125I-HEAT or 3H-yohimbine were not significantly different between BBM and BLM. These results indicate that both types of α-adrenoceptors seem to be localized largely in the BLM.View full abstractDownload PDF (259K) -
Kunihiko YOKOTANI, Yasunobu OKUMA, Yoshitsugu OSUMI1987 Volume 45 Issue 2 Pages 288-291
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effect of intracerebroventricularly (i.c.v.) administered nicotine was investigated in urethane-anesthetized rats. I.c.v., but not intravenously, administered nicotine (300 and 600 nmole/animal) inhibited the increase in gastric acid output induced by electrical stimulation of the vagus nerve. This antisecretory effect of nicotine was abolished by combined pretreatment with adrenalectomy and 6-hydroxydopamine (50 mg/kg, i.v., 3 days before). I.c.v.-administered nicotine also raised the blood levels of catecholamines. These observations suggest that i.c.v. administered nicotine leads to excitation of the central sympatho-adrenomedullary outflow and inhibits gastric acid output induced by stimulation of the vagus nerve.View full abstractDownload PDF (215K) -
Masanobu NAKAHIRO, Nobuo NISHI, Isao FUKUCHI, Daisuke MOCHIZUKI, Susum ...1987 Volume 45 Issue 2 Pages 292-294
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe interactions of the “antidementia drug” pantoyl-γ-aminobutyric acid (pantoyl-GABA) with γ-aminobutyric acid (GABA) receptors were investigated by studies on bindings of radiolabelled ligands in rat brain. Pantoyl-GABA inhibited the binding of [3H]GABA to GABAA receptors and those of [3H]baclofen and [3H]GABA to GABAB receptors in the rat cerebral cortex. These data suggest that pantoyl-GABA interacts with both types of GABA receptors in the rat brain.View full abstractDownload PDF (161K)
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