巻号一覧
53 巻 (1990)
- 4 号 p. 419-
- 3 号 p. 285-
- 2 号 p. 135-
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53 巻, 2 号
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Shigetoshi CHIBA, Miyoko TSUKADA1990 年 53 巻 2 号 p. 135-143
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーUsing the cannula inserting method, vasodilator responses to alpha2-adrenoceptor agonists (clonidine, guanabenz, DJ7141 and xylazine) were investigated in isolated and perfused rat common carotid arteries. Alpha2-adrenoceptor agonists dose-dependently induced a vasodilation in preparations preconstricted by noradrenaline. The potencies were in the order of clonidine>guanabenz>DJ-7141 ≥ xylazine. Removal of the endothelium inhibited ACh-induced vasodilation, but not the alpha2-agonist-induced dilation. Atropine treatment inhibited AChinduced vasodilation, but not the alpha2-agonist-induced dilation. Alpha2-agonist-induced dilations were not modified by beta-blockade, which significantly suppressed isoprenaline-induced vasodilations. The potent alpha2-adrenoceptor antagonist DG5128 did not influence the alpha2-agonist-induced vasodilation. In preparations preconstricted by PGF2α, clonidine and xylazine never induced a vasodilation, and clonidine frequently induced vasoconstrictions that were completely blocked by bunazosin. It is concluded that alpha2-adrenoceptor agonist-induced vasodilation is independent from the existence of the endothelium, and that it is not related to vascular beta- and alpha2-adrenoceptors and muscarinic receptors, suggesting that the alpha2-adrenoceptor agonist-induced vasodilation is due to an antagonistic activity towards the vascular alpha1 -adrenoceptors.抄録全体を表示PDF形式でダウンロード (456K) -
Kazuichi NATORI, Yuko OKAZAKI, Tsunemasa IRIE, Junki KATSUBE1990 年 53 巻 2 号 p. 145-155
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーThe effects of the compound SM-10888 (9-amino-8-fluoro-1, 2, 3, 4, -tetrahydro-2, 4-methanoacridine citrate) in a number of pharmacological and biochemical tests were studied and compared to those of tacrine (THA), amiridin, HP-029 and physostigmine. SM-10888 inhibited cholinesterase activity (IC50: 2.3 × 10-7 M) in rat cortical P2 fraction with almost the same potency as THA, while SM-10888 was 2-4 times more potent than amiridin and HP-029, but about 10 times less potent than physostigmine. When given to mice p.o., SM-10888 induced central (hypothermia) and peripheral (salivation) cholinergic effects. When the ratio of the ED50 value for hypothermia to that for salivation was regarded as the index of the selectivity to the central nervous system (CNS), SM-10888 was shown to be about 3 times more selective to the CNS than the other four drugs in mice. The minimum effective dose of SM-10888 for its increasing effect on acetylcholine (ACh) content in the mouse cerebral cortex was about 10 times higher than that of physostigmine, but 5-10 times lower than those of THA, amiridin and HP029. These results suggest that SM-10888 is an adequate drug for increasing the brain ACh content with less peripheral cholinergic side effects than THA, amiridin, HP-029 and physostigmine.抄録全体を表示PDF形式でダウンロード (520K) -
Kiyokazu NAKASE, Ikuko KIMURA, Masayasu KIMURA1990 年 53 巻 2 号 p. 157-164
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーThe contracting or inhibitory effects of pollen-extract components, diamines and derivatives of feruloylputrescine (FP) were investigated on the isolated bladder or urethral smooth muscles of mice. Among the nine diamines (NH2•(CH2)n·NH2, n=2-10) tested, five of them with shorter carbon chains (n=2-6) (0.1-30.0 mM) only slightly contracted the bladder strips and to some extent inhibited the noradrenaline (NA, 1.77 μM)-induced contraction of urethral strips. 1, 5-Diaminopentane (C5), a component of the pollen-extract, inhibited most effectively the NA-induced contraction of urethral strips with an IC50 value of 2.3 mM (95% confidence limit: 2.0-2.6 mM). FP, also a component of the pollenextract, inhibited the NA-induced contraction of urethral strips in a non-competitive manner, producing 32.5±5.5% (N=5) inhibition at 378 μM. Among the derivatives of FP, feruloylcadaverine inhibited urethral contraction most potently, producing 46.3±7.1% (N=5) inhibition at 359 μM. These derivatives had no effect on bladder contraction. In contrast, four diamines with longer carbon chains (n=7-10) contracted the bladder strips (3-30 mM) and potentiated the NA-induced contraction of urethral strips (10 μM-3 mM). Thus, the components of the pollenextract, FP and C5, potently inhibited urethral contraction, which may facilitate the discharge of urine in vivo.抄録全体を表示PDF形式でダウンロード (338K) -
Toshiyuki SAITO, Yoshimasa KURATA, Kazu TAKENO1990 年 53 巻 2 号 p. 165-173
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーThe effect of braxin A1, a new bracken glucoside, on histamine release from isolated rat peritoneal mast cells was studied. Braxin A1 caused the release of histamine in a dose-dependent manner; the release was slow and increased gradually with time, finally reaching a maximum release of 100%. The action of braxin A1 depended on the incubation temperature in the range from 4°C to 49°C, while it was almost abolished at 0°C. The action of braxin A1 was unaffected by removing calcium or any inorganic ions from the incubation medium and by the addition of 2, 4-dinitrophenol or theophylline. The mast cells exposed to braxin A1 were vitally stained with trypan blue and swelled greatly. The cell swelling was characterized by the protrusion of swollen cytoplasmic granules. The present results for braxin Al were similar to those for the ionophore X537A except for the extracellular inorganic ion dependency, but they were different from those observed with compound 48/80. These results suggest that braxin A1 releases histamine from mast cells without both exocytosis and membrane lysis, but with a cytotoxic action on cytoplasmic membranes by a different mode of action from that of X537A.抄録全体を表示PDF形式でダウンロード (627K) -
Shuichi KOIZUMI, Yasufumi KATAOKA, Kazuto SHIGEMATSU, Masami NIWA, Sho ...1990 年 53 巻 2 号 p. 175-183
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーEffect of WEB 1881 FU on hypoglycemia/hypoxia-induced brain damage in rats was evaluated and compared to findings obtained with idebenone. We used an in vitro model that facilitated the direct monitoring of dopamine release from striatal slices. The response to high K+ stimulation under perfusion of the slices with D-glucose-free Ringer solution (hypoglycemia) decreased at 40 min, and then practically disappeared. WEB 1881 FU at 10-6 M or idebenone at 10-6 M significantly protected against impairment of the striatal responses under the conditions of hypoglycemia. Hypoglycemic injury, evidenced by a remarkable neuron loss, necrosis and spongyosis was also ameliorated by these drugs. WEB 1881 FU at 10-6 M had a protective action against the impairment of striatal responses evoked by NaCN (electron transport inhibitor at site 3) and oligomycin (inhibitor of mitochondrial ATP synthesis), but idebenone at 10-6 M did not. In light of these observations, the possibility that WEB 1881 FU and idebenone exert neuroprotective actions against hypoglycemic/hypoxic brain injury by activating energy metabolism with different mechanisms from each other has to be considered.抄録全体を表示PDF形式でダウンロード (608K) -
Yuji ABE, Akihiro NARIMATSU, Akihiro TOBE1990 年 53 巻 2 号 p. 185-194
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーThe effects of betaxolol, a cardioselective beta-adrenoceptor antagonist, on ischemic myocardial acidosis were studied in dog hearts, in which the left anterior descending coronary artery was partially occluded for 90 min, and were compared with those of atenolol and propranolol. Myocardial ischemia produced a decrease in myocardial pH (measured by a micro glass pH electrode) and an elevation of the ST segment of epicardial ECG (assessed by a surface electrode). Betaxolol (0.01, 0.03 or 0.1 mg/kg), atenolol (0.03 or 0.1 mg/kg) or propranolol (0.03 or 0.1 mg/kg), when injected i.v. 30 min after ischemia, restored myocardial pH and the ST segment of ECG that had been altered by partial occlusion. However, the effect of betaxolol on myocardial acidosis was more potent than that of atenolol or propranolol. The decrease in (+)dp/dt by betaxolol (0.03 mg/kg) was less potent than that by atenolol (0.1 mg/kg) and equivalent to that by propranolol (0.1 mg/kg), although the restorations of myocardial acidosis by the drugs were almost equivalent. These results have confirmed that beta-adrenoceptor antagonists attenuate the ischemiainduced myocardial acidosis and have shown that among three beta-adrenoceptor antagonists, betaxolol is the most effective in improving myocardial acidosis with a relatively weak effect on myocardial contractile function.抄録全体を表示PDF形式でダウンロード (416K) -
Mei Lin GO, How Sung LEE1990 年 53 巻 2 号 p. 195-199
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーThe effects of the antimalarial agent mefloquine on the release of marker enzymes, acid phosphatase and beta glucuronidase, from the rat liver lysosomes in a crude lysosomal preparation were investigated and compared with that of chloroquine whose membrane effects have been well-documented in the literature. At 10 μM, mefloquine decreased significantly the release of marker enzymes when compared to the control, but at the higher concentrations of 100 μM and 500 μM, it markedly accelerated the release of enzymes. This suggested that mefloquine exerted a concentration-dependant biphasic effect of membrane stabilization and labilization. In comparison, chloroquine diminished the release of enzymes over the concentration range of 10-500 μM, that is showing a membrane stabilizing effect similar to other reports. Since serum levels of 1.6-3.2 μM are reported after a weekly dose of mefloquine, the present results suggest that a predominant stabilization effect should prevail under these conditions. However, higher drug concentrations may result in labilization with undesirable consequences.抄録全体を表示PDF形式でダウンロード (286K) -
Masami KUBO, Jyouji KATO, Takashi OCHIAI, Ryuichi ISHIDA1990 年 53 巻 2 号 p. 201-210
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーTA-6366 and its active metabolite 6366A inhibited swine renal angiotensin converting enzyme (ACE) activity with IC50s of 9900 and 2.6 nM, respectively. TA-6366 (0.05-0.5 mg/kg, p.o.) inhibited the angiotensin I (AT-I)-induced pressor response in rats. 6366A augmented bradykinin (BK)-induced contraction of guinea pig ileum more potently than captopril. However, when the augmentation on BK-induced hypotension in rats was used as an indicator, TA-6366 was less active than captopril. TA-6366 increased plasma renin activity and plasma AT-I concentration. Oral administration of TA-6366 lowered the blood pressure in two-kidney one-clip renal hypertensive rats at 0.5 to 2 mg/kg and in spontaneously hypertensive rats (SHRs) at 2 to 10 mg/kg. The antihypertensive effect of TA-6366 was approximately 5 times more potent than that of captopril and almost as potent as that of enalapril. In SHRs, the antihypertensive action of TA-6366 was intensified in potency when administered repeatedly. The duration of action was longer than those of captopril and enalapril. However, TA-6366 had no substantial effect on the blood pressure in DOCA/saline hypertensive rats. These results indicate that TA-6366 is a potent and long lasting antihypertensive agent and that its antihypertensive action is attributable to the inhibition of ACE.抄録全体を表示PDF形式でダウンロード (530K) -
Yuko OKAZAKI, Kazuichi NATORI, Tsunemasa IRIE, Junki KATSUBE1990 年 53 巻 2 号 p. 211-220
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーThe effects of the tacrine (THA) derivative SM-10888 (9-amino-8-fluoro-1, 2, 3, 4-tetrahydro-2, 4-methanoacridine citrate) on habituation and passive avoidance responses were studied in mice. We examined its effects on habituation of exploratory activity, measured by photo-cell beam interruptions in a small, simple cage and cycloheximide (CXM)- or electroconvulsive shock (ECS)-induced stepdown type passive avoidance response (PAR) failures in comparison with those of THA, amiridin, HP-029 and physostigmine. SM-10888 (6 mg/kg, p.o.) administered post-acquisition session enhanced the retention of habituation. CXM and ECS-induced PAR failures were improved by SM-10888 (6 mg/kg, p.o.) administered at pre-training or post-training, respectively. THA enhanced the retention of habituation and improved CXM-induced PAR failure at 30 mg/kg, p.o., but did not affect ECS-induced PAR failure at 1-15 mg/kg, p.o. Amiridin and HP-029 were also effective on habituation and CXM-induced PAR failure at 40-50 mg/kg, p.o., but did not affect ECS-induced PAR failure at the tested doses. Physostigmine showed a moderate improvement only in CXM-induced PAR failure. The results indicate that SM-10888 enhanced habituation and improved PAR failures at much lower doses than THA. This seems to depend on its high selectivity to the central nervous system.抄録全体を表示PDF形式でダウンロード (543K) -
Kazuho ABE, Megumi TAKAYANAGI, Hiroshi SAITO1990 年 53 巻 2 号 p. 221-227
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーNeurotrophic effects of recombinant human basic fibroblast growth factor (hbFGF) and its modified protein CS23 on brain neurons were evaluated by their abilities to promote survival of primary cultured neurons from various regions of fetal rat brain. In the molecule of CS23, two serines are substituted for two cysteines at positions 70 and 88 in the natural hbFGF. Both hbFGF and CS23 markedly increased the survival of cultured neurons from all regions tested, i.e., cerebral cortex, septum, striatum, hippocampus, thalamus, substantia nigra, colliculus and cerebellum. The effects were concentration-dependent, in the range of 0.01 to 10 ng/ml, in similar manners among all regions. Although the maximal number of surviving neurons in the presence of CS23 was little different from that of hbFGF, CS23 could significantly promote neuronal survival at a lower concentration than hbFGF. The time-course of these effects on survival was almost the same between hbFGF (1 ng/ml) and CS23 (1 ng/ml). These results suggest that hbFGF has a strong neurotrophic activity on a wide range of brain neurons and that CS23 maintains the activity of original hbFGF successfully.抄録全体を表示PDF形式でダウンロード (540K) -
Xiao-Ming ZHOU, Shuji UCHIDA, Atsushi MIZUSHIMA, Hiroshi YOSHIDA1990 年 53 巻 2 号 p. 229-234
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーStimulation of phosphoinositide hydrolysis by carbachol was studied in slices of guinea pig cerebral cortex under normal conditions (4.7 mM K+) and depolarization conditions with high K+ (42 mM K+). Slices were labeled with [myo-3H]-inositol, and the effects of carbachol and high K+ on the formation of inositol-bisphosphates (IP2) and inositol-trisphosphates (IP3) were determined. Carbachol (10 mM) caused only 140% stimulation of the formations of IP2 and IP3 over the control value in normal Krebs Ringer Buffer (KRB), but about 200% stimulation in high K+ medium. Dose-response curves for the effect of carbachol on the formations of IP2 and IP3 showed that high K+ medium selectively decreased the ED50 value of carbachol for IP2 formation about 3-fold. A Ca++ channel blocker, verapamil, inhibited the synergistic effect of carbachol and high K+ on IP2 formation, and a decrease in extracellular Ca++ also inhibited IP2 formation induced by high K+, but these treatments had little, if any, effect on IP3 formation. The possibility that IP2 may be directly generated by hydrolysis of phosphatidylinositol 4-monophosphate (PIP) as well as from hydrolysis of IP3 was discussed.抄録全体を表示PDF形式でダウンロード (355K) -
Takeshi SAKAI1990 年 53 巻 2 号 p. 235-246
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーEffects of acetylcholine (ACh) on the membrane potential and current recorded from endothelial cells dispersed from the rabbit aorta were investigated using the patch-clamp technique. ACh hyperpolarized the endothelial cell membrane. Using the whole-cell voltage-clamp procedure, ACh (10-6 M) induced an outward current, and this current was blocked by atropine (10-6 M). Application of either pirenzepine (3×10-7 M) or AF-DX 116 (3×10-6 M) slightly inhibited the ACh-induced outward current, and simultaneous application of these two blockers markedly inhibited the outward current. Application of caffeine (2×10-2 M), ryanodine (10-5 M) or heparin (10-5 g/ml) reduced the amplitude of the AChinduced outward current. A single-channel current recording using the patchclamp technique revealed that ACh opens a Ca-dependent K-channel with a singlechannel current conductance of 9 pS. These results indicate that both M1 and M2 receptor subtypes are present in endothelial cells of the rabbit aorta and that ACh activates the Ca-dependent K channel via release of Ca from intracellular store sites. In addition, methylene blue inhibited the ACh-induced outward current from the outside membrane.抄録全体を表示PDF形式でダウンロード (608K) -
Hideaki HARA, Hiroshi ONODERA, Haruo NAGASAWA, Kyuya KOGURE1990 年 53 巻 2 号 p. 247-253
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーA novel transient middle cerebral artery (MCA) occlusion model in the rat was used to evaluate the effect of nimodipine on brain edema and mortality. Nimodipine (30 μg/kg) administered immediately after 3 hr of transient unilateral MCA occlusion attenuated significantly the post-ischemic increase of tissue water content and partly attenuated 45Ca accumulation in the parieto-temporal cortex ipsilateral to the left MCA occlusion 3 hr after reperfusion. Nimodipine decreased the mortality rate at 6 and 9 hr after recirculation, although the survival rate at 24 hr after recirculation was not different from the control group. These results suggest that nimodipine has beneficial effects in the early phase of the reperfusion period.抄録全体を表示PDF形式でダウンロード (592K) -
Toshio FUJIYOSHI, Masaharu DOZEN, Hiroyuki IIDA, Kenro IKEDA, Izumi HA ...1990 年 53 巻 2 号 p. 255-258
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーUsing a bradykinin enzyme immunoassay, we measured the amount of kinin in the peritoneal washings of mice with the kaolin-induced writhing reaction. Simultaneous treatment with captopril, a kininase II inhibitor, significantly increased the kinin level at 1 min after kaolin injection. Soybean trypsin inhibitor injected simultaneously with kaolin almost completely suppressed the kinin level at 1 min with or without treatment of captopril. These results suggest that kinin is released through activation of the plasma kallikrein-kinin system by kaolin, and that kinin could be a main mediator for the writhing reaction.抄録全体を表示PDF形式でダウンロード (206K) -
Ryosuke YORIKANE, Hiroyuki KOIKE1990 年 53 巻 2 号 p. 259-263
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーEndothelin (ET) was administered into the coronary ostia at doses of 0.1-1 μg/kg in anesthetized rats. The ST segment was depressed at doses below 0.5 μg/kg and was transiently elevated at 1 μg/kg. Ventricular arrhythmias developed at doses above 0.5 μg/kg. The arrhythmias that developed at 1 μg/kg were precipitated into ventricular fibrillation. At the time when the arrhythmias developed, the ischemic changes had already subsided. These results suggest that ET may have an arrhythmogenic action, which is not solely attributable to myocardial ischemia.抄録全体を表示PDF形式でダウンロード (233K) -
Kiyoshi OIZUMI, Masaaki MIYAMOTO, Hiroyuki KOIKE1990 年 53 巻 2 号 p. 264-266
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーCS-905, (±)-3-(1 -diphenylmethylazetidin-3-yl)5-isopropyl 2-amino-1, 4-dihydro-6-methyl-4-(m-nitrophenyl)-3, 5-pyridine-dicarboxylate, is a novel dihydropyridine calcium blocker. Both CS-905 and nicardipine, when administered orally, produced a dose-dependent fall of blood pressure in conscious perinephritic hypertensive dogs. Unlike the hypotensive effect of nicardipine, that of CS-905 has a gradual onset and is long-lasting, with little increase in the heart rate and plasma renin activity (PRA). The lack of both tachycardia and increase of PRA is probably mostly due to the slow onset of antihypertensive action following CS-905.抄録全体を表示PDF形式でダウンロード (181K) -
Shigetoshi CHIBA, Miyoko TSUKADA1990 年 53 巻 2 号 p. 267-270
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーUsing the cannula inserting method, we investigated the vascular responses to norepinephrine (NE), phenylephrine and isoprenaline (Isp) in isolated, perfused simian facial veins. NE usually induced only a vasodilation in nonpreconstricted veins. Phenylephrine consistently induced only a slight vasoconstriction, and Isp produced only a vasodilation. NE-induced vasodilations were reversed to vasoconstrictions after treatment with a relatively larger dose of propranolol. It is concluded that simian facial veins have a spontaneous intrinsic tone and dominant abundant beta-adrenoceptors but sparse alpha1 -adrenoceptors.抄録全体を表示PDF形式でダウンロード (210K) -
Nobuyuki HARA, Youichi HARA, Yasuhiro NATSUME, Yoshiaki GOTO1990 年 53 巻 2 号 p. 271-274
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーAcid secretagogue effects of central and peripheral baclofen were compared in the rat. Intravenously (0.1-1.0 mg/kg) and intracerebroventricularly (0.1-1.0, μg) administered baclofen augmented acid output to the same degree in a dose-dependent manner. GABA microinjected into the lateral hypothalamus (200 and 400 μg) significantly increased acid output. These support the proposal that baclofen stimulates acid secretion through central mechanisms and also the possible role of GABA in central regulation mechanisms of acid secretion.抄録全体を表示PDF形式でダウンロード (195K) -
Koichi SHIMOHARA, Hiromichi NIIDA, Susumu OKABE1990 年 53 巻 2 号 p. 275-279
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーEffects of a newly synthesized compound, KB-5492, on gastric lesions and gastric secretion were studied in rats. Oral KB-5492 inhibited the lesions induced by HCl·ethanol, HCl·aspirin, water-immersion stress, indomethacin, histamine and prednisolone at 30-300 mg/kg. The ED50 values varied from about 35 to 98 mg/kg. KB-5492 had no effect on gastric acid secretion even at 300 mg/kg. KB-5492 appeared to have a much more potent protective effect than a known anti-ulcer drug, sofalcone, against acute gastric lesions.抄録全体を表示PDF形式でダウンロード (268K) -
Noboru TODA, Hiroshi BABA, Tomio OKAMURA1990 年 53 巻 2 号 p. 281-284
発行日: 1990年
公開日: 2006/07/11
ジャーナル フリーTransmural electrical stimulation caused a relaxation in the dog duodenal longitudinal muscle strips treated with atropine, phentolamine and propranolol, which was abolished by tetrodotoxin. The relaxation was suppressed by oxyhemoglobin and L-NG-nitro-arginine (L-NA), but not influenced by D-NA. Inhibition by L-NA was reversed by L-arginine, but not by D-arginine. The response to transmural electrical stimulation was similar to that caused by nitric oxide or nitroglycerin. Nitric oxide appears to participate importantly in non-adrenergic, non-cholinergic nerve-mediated relaxation.抄録全体を表示PDF形式でダウンロード (155K)
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