巻号一覧
57 巻 (1991)
- 4 号 p. 455-
- 3 号 p. 263-
- 2 号 p. 127-
- 1 号 p. 1-
57 巻, 3 号
選択された号の論文の22件中1～22を表示しています
- |<
- <
- 1
- >
- >|
-
Sen Kau, Christopher Yochim, My Linh Do, Krystyna Leszczynska, Chester ...1991 年 57 巻 3 号 p. 263-277
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーICI 181, 037, the most active compound from a series of 1, 1-diaryl-carbin-1-ol-2 amines, was evaluated for diuretic and cardiovascular activity. In saline-loaded rats, the magnitude of water diuresis and saluresis produced by ICI 181, 037 (10 mg/kg, p.o.) was equal to that of hydrochlorothiazide. Water diuresis and saluresis produced by ICI 181, 037 were enhanced with SKF 525A, ampicillin or neomycin plus lincomycin, suggesting that ICI 181, 037 is an active diuretic. In conscious dogs, the saluretic activity of ICI d-181, 037 (5 mg/kg, p.o.) was about 80% of the corresponding hydrochlorothiazide value, whereas the 1-isomer demonstrated only minimum saluretic activity. In both rats and dogs, the concurrent kaliuresis after ICI 181, 037 or its enantiomers was minimal as compared to hydrochlorothiazide. Following chronic dosing with diuretic doses, the basal levels of plasma potassium in dogs were not altered. In amphibian in vitro models for mimicking mammalian nephron, ICI 181, 037 and its enantiomers demonstrated antinatriferic and antichloriferic activities, suggesting multiple renal sites of action for this agent. Racemic ICI 181, 037 and its isomers reversed ouabain-induced arrhythmia in dogs and/or reduced the ouabain-induced mortality in mice after intravenous administration. It is concluded that ICI 181, 037, particularly its d-isomer, is a novel eukalemic diuretic and possesses antiarrhythmic activity.抄録全体を表示PDF形式でダウンロード (789K) -
Kumiko Sugisawa, Seiichi Komori, Tadashi Takewaki, Hidenori Ohashi1991 年 57 巻 3 号 p. 279-289
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーIntestinal segments obtained from guinea pig ileum were set up in an organ bath to record peristaltic responses to distension by a pressure rise in the lumen. The effects of drugs applied in the bathing medium on the peristaltic responses were examined. Sodium nitroprusside (10-9M to 10-5M) stimulated the peristaltic reflex. Nitroglycerin (10-7 M) was similarly effective in stimulating the peristalsis. A permeable cyclic GMP, 8-bromo cyclic GMP (2.5 × 10-4 M), mimicked the action of these compounds. Methylene blue (10-5 M) blocked the nitroprusside-induced stimulation of the peristalsis, but not the effect of 8-bromo cyclic GMP. Sodium nitroprusside did not change the baseline tension of the circular muscle, and it enhanced neither the contractile response to electrical direct stimulation nor the cholinergic transmission to the circular muscle. These results suggest that nitric oxide is formed from the nitrocompounds in mechanosensitive neurons in the intestine and causes activation of guanylate cyclase by which the level of intracellular cyclic GMP is elevated, and cyclic GMP acts to make the stretch receptors more sensitive. As nitric oxide is derived from the enteric vascular bed or neurons, its importance as a modulator of peristaltic activity in the intestine is discussed.抄録全体を表示PDF形式でダウンロード (508K) -
Fumitoshi Asai, Takeshi Oshima1991 年 57 巻 3 号 p. 291-298
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーPathophysiological and therapeutic properties of anemia in rats with adjuvant-induced arthritis (AA) were investigated. Both anemia and chronic inflammation were induced in rats by a single injection of Freund's complete adjuvant. This study confirmed other earlier data that these anemic rats with AA had reduced serum iron levels and that the anemia was characterized as mild, non-progressive, hypochromic, microcytic. In addition, our studies showed that these anemic rats had slightly but significantly enhanced erythropoietin titers, but not renal failure; there was no significant difference in blood urea nitrogen and creatinine levels in anemic and normal groups. The anemia in rats with AA was improved by recombinant human erythropoietin (r-HuEPO) at 30 and 100 U/kg/day, given i.v. for 5 days. In contrast, iron-chondroitinsulfate colloid (10 mg/kg/day, i.v. for 5 days) failed to improve the anemia and to enhance the effects of r-HuEPO. These data suggest that anemia in rats with adjuvant-induced arthritis is distinguished, pathophysiologically and therapeutically, from iron deficiency anemia, hemolytic anemia, and renal anemia.抄録全体を表示PDF形式でダウンロード (379K) -
Koji Takeuchi, Hideyuki Nishiwaki, Hiromichi Niida, Koji Ueshima, Susu ...1991 年 57 巻 3 号 p. 299-310
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーPathogenesis of duodenal ulcers induced by diethyldithiocarbamate (DDC), a superoxide dismutase (SOD) inhibitor, was investigated in the rat. Repeated s.c. administration of DDC (750 mg/kg) every 12 hr induced duodenal ulcers in the fed rats, and the severity of the ulcers reached the maximum after three injections. DDC not only reduced basal acid output but also impaired duodenal alkaline secretion. These ulcers were significantly prevented by antioxidative agents such as SOD (50000 units/kg, s.c.), allopurinol (50 mg/kg, s.c.) or glutathione (200 mg/kg, s.c.) as well as the antisecretory agent cimetidine (100 mg/kg, s.c.). The impaired HCO3- response caused by DDC was partially but significantly reversed by either SOD (15000 units/kg/hr, i.v.), allopurinol or glutathione; and SOD by itself significantly elevated the rate of basal alkaline secretion. 16, 16-Dimethyl prostaglandin E2 (10 μg/kg, s.c.) increased duodenal HCO3 output in the presence of DDC and significantly prevented the development of duodenal ulcers in response to DDC. These results suggest that the mucosal antioxidative system including SOD may play a role in the regulatory process of alkaline secretion and contribute to the mucosal defensive ability in the duodenum. The insufficiency of this system may be involved in the pathogenesis of DDC-induced duodenal ulcers.抄録全体を表示PDF形式でダウンロード (692K) -
Toshitaka Nabeshima, Eiko Maruyama, Akira Katoh, Tsutomu Kameyama1991 年 57 巻 3 号 p. 311-319
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe effects of 9-amino-1, 2, 3, 4-tetrahydroacridine (tacrine), an active acetylcholinesterase inhibitor, on cycloheximide- and basal forebrain (BF) lesion-induced memory deficit in the water maze and passive avoidance task were investigated. While cycloheximide (1.5 mg/kg, s.c.) produced amnesia in the passive avoidance task, chronic administration of tacrine (1, 3 and 10 mg/kg, once a day for 1 week) improved the amnesia. BF lesion produced amnesia in both the water maze and passive avoidance tasks. Chronic tacrine (0.1-3 mg/kg, passive avoidance task, or 0.3 mg/kg, water maze task, once a day for 1 week) improved BF lesion-induced amnesia in the passive avoidance and water maze tasks. These results suggest that tacrine may be useful for senile dementia.抄録全体を表示PDF形式でダウンロード (447K) -
Fusao Ueda, Takashi Kyoi, Kiyotaka Mimura, Kiyoshi Kimura, Masao Yamam ...1991 年 57 巻 3 号 p. 321-328
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe effects of drugs related to cyclic AMP and a tumor promoter, phorbol ester, on intercellular communications via gap junctions were investigated by the Lucifer Yellow-transfer method in cultured rabbit gastric epithelial cells. Cells were in contact with each drug for 4 hr before the microinjection of the dye into a cell. Dye transfer capacity was significantly increased by dibutyryl cyclic AMP (10-3 M), theophylline (10-3 M), 3-isobutyl-1-methylxanthine (10-4 M), forskolin (10-6 M) and irsogladine (10-4 M); and it was inhibited by 12-O-tetradecanoyl-phorbol-13-acetate (100 ng/ml). These results suggest that the intercellular communication between cultured rabbit gastric epithelial cells is upregulated by cyclic AMP.抄録全体を表示PDF形式でダウンロード (898K) -
Akane Ishihara, Hiroshi Saito, Hiroyuki Ohta, Nobuyoshi Nishiyama1991 年 57 巻 3 号 p. 329-336
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーEffects of the basal forebrain (BF) lesion on memory and learning performances were investigated in mice. Eight-week-old male mice received bilateral BF lesion by delivering a radiofrequency current. From fifteen days after the surgery, the step through type passive avoidance task was performed daily for 10 days. Lesioned animals showed severe impairment in the acquisition process of this task, but not in the retention process. Ambulatory activity of the BF-lesioned mice did not differ from those of the control group, suggesting the observed learning impairment was not due to the alteration of motor activity. These results indicate that a memory impaired model mice can be successfully made by the radiofrequency lesion of bilateral BF neurons.抄録全体を表示PDF形式でダウンロード (565K) -
Toru Yamashita, Yukinori Masuda, Toshinori Sakai, Sakuya Tanaka, Yutak ...1991 年 57 巻 3 号 p. 337-348
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe correlation between the binding of NZ-105, a newly synthesized 1, 4-dihydropyridine (DHP) derivative, on DHP receptors and its inhibitory activity on transmembrane 45Ca2+ uptake was investigated. 3H-NZ-105 bound rabbit aortic microsomes more slowly than did 3H-nitrendipine (3H-NTD): the association and dissociation rate constants of 3H-NZ-105 were about 70 times and 10 times less than those of 3H-NTD, respectively. The dissociation constant (Kd) of 3H-NZ-105 (4.48 nM) was about 6 times larger than that of 3H-NTD (0.79 nM), and the maximum number of binding sites (Bmax) for 3H-NZ-105 (112.5 fmoles/mg protein) was about the same as that for 3H-NTD (106.2 fmoles/mg protein). Unlabelled NZ-105 and nicardipine fully, and in a concentration-dependent manner, displaced 3H-NZ-105 specific binding. Pre-incubation with NZ-105 also concentration-dependently (more than 0.1 μM) inhibited the transmembrane 45Ca2+ uptake increment induced by a high-K+ (50 mM) solution. The inhibitory efficacy of NZ-105 became larger as the incubation period with this compound increased (from 1 hr incubation to 3 hr incubation), and recovery was difficult even after washout for 3 hr. Based on these results, we conclude that NZ-105 causes blockade of voltage-dependent calcium channels (VDCs) by binding to DHP receptors. Moreover, the very slow onset and recovery from NZ-105-induced vasodilation may be attributable to the slow and long-lasting inhibition of transmembrane calcium uptake, which accompanies its very slow binding to and dissociation from DHP receptors.抄録全体を表示PDF形式でダウンロード (625K) -
Haruaki Ninomiya, Motohatsu Fujiwara1991 年 57 巻 3 号 p. 349-354
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーEpithio-11, 12-methano-thromboxane A2 (STA2), a stable analog of thromboxane A2 (TXA2), stimulated inositol phosphates (IPs) accumulation in canine mesenteric artery strips, but not in cerebral (basilar) artery strips. When canine mesenteric artery strips were incubated with 0.1 μM [3H]myo-inositol for 15 min and then stimulated with 10 μM STA2 for 30 min, there was a significant increase in 3H-IPs accumulation as measured by anion exchange chromatography (2, 028 ± 204 and 3, 526 ± 210* dpm/mg protein for basal and stimulated accumulations, respectively; means ± S.E.M., n = 3, *P < 0.01, significantly different from the basal value). This effect of STA2 was dose-dependent with an EC50 value of 1.6 ± 0.2 μM. The presence of equimolar concentrations of TXA2 receptor antagonists, either ONO-3708 (9, 11-dimethylmethano-11, 12-methano-13, 14-dihydro-13-aza-14-oxo-15-cyclopental-16, 17, 18, 19, 20-pentanor-15-epi-thromboxane A2) or S-1452 (5Z-7-(3-endo-phenylsulfonylamino (2.2.1.)-bicyclohept-2-exo-yl)heptenoic acid), completely blocked the effect of STA2. These results suggest the presence of TXA2 receptors coupled with IPs accumulation in canine mesenteric artery strips. The exact location of the TXA2 receptor-IPs system, however, remains unknown.抄録全体を表示PDF形式でダウンロード (300K) -
Tohru Masukawa, Yoshihiro Tochino1991 年 57 巻 3 号 p. 355-359
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe circadian variation of decapitation-induced gasping was investigated by measuring the gasping duration of isolated mouse head after decapitation under both normal and restricted feeding conditions. In the normally fed mice, there was a circadian periodicity in the gasping duration: it was longer during the light period than during the dark period. The circadian periodicity was completely reversed by the restriction of food. The circadian periodicities of the gasping duration were conversely parallel to those of body temperature in both normal and feeding restricted mice, and regression analysis revealed a negative correlation between the gasping duration and body temperature. Furthermore, pentobarbital and ethanol, agents that caused hypothermia, markedly prolonged the gasping duration. These findings suggest that there is a circadian periodicity in the brain reactivity after complete ischemia, which may be associated with the changes of body temperature.抄録全体を表示PDF形式でダウンロード (231K) -
Eriko Aizu, Satoshi Yamamoto, Kiyotaka Nishikawa, Ryuichi Kato1991 年 57 巻 3 号 p. 361-366
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe tumor promoter anthralin stimulated prostaglandin E2 (PGE2) and arachidonic acid release from primary cultures of mouse epidermal cells. Epidermal growth factor (EGF) hardly stimulated PGE2 release by itself; however, a combination of anthralin and EGF synergistically stimulated PGE2 release. Neither anthralin, EGF nor EGF plus anthralin affected the incorporation of arachidonic acid into cellular phospholipids at least up to 2 hr after the stimulation by these agents. In the presence of EGF, however, [3H]arachidonic aicd in the medium decreased substantially 4 -8 hr after the addition of this agent, indicating that EGF suppresses [3H]arachidonic acid release and stimulates the incorporation of [3H]arachidonic acid into the cells during this time period. Cellular cyclooxygenase activity was increased by treating the cells either with anthralin or EGF, and it was synergistically increased by EGF plus anthralin. Both cycloheximide and actinomycin D inhibited the increase in cyclooxygenase activity caused by EGF plus anthralin. These results indicate that the synergistic stimulation of PGE2 release caused by EGF plus anthralin is due to a synergistic stimulation of arachidonic acid release (in the early phase of stimulation) and a synergistic increase in cyclooxygenase activity, probably a synergistic induction of cyclooxygenase, by these agents.抄録全体を表示PDF形式でダウンロード (312K) -
Toshiji Sugai, Kazuko Kojima, Naomi Iwakami, Yoshikuni Suzuki1991 年 57 巻 3 号 p. 367-375
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーVasorelaxant and hypotensive effects of tilisolol hydrochloride (N-696) in isolated rat thoracic aorta and pithed rats were investigated. In rat thoracic aorta pre-contracted with KCl (20 mM), tilisolol (10-5-10-3 M) produced concentration-related relaxation, but nadolol and atenolol did not significantly inhibit the responses to 20 mM KCl. The concentration-relaxation curve of tilisolol underwent rightward parallel shifts only to a limited extent in the presence of glibenclamide, a specific antagonist of K+ channel openers. Glibenclamide also shifted the concentration-relaxation curve of cromakalim to the right and in a parallel manner, whereas it did not change that of propranolol. In pithed rats, tilisolol (0.5-2.0 mg/kg, i.v.), but neither nadolol nor atenolol, caused a dose-dependent decrease in diastolic blood pressure and a slight increase in heart rate. Following treatment of the preparation with glibenclamide, the hypotensive effects of tilisolol and cromakalim were antagonized, while that of propranolol was not affected. These results suggest that the vasorelaxant and hypotensive actions of tilisolol involve an opening of K+ channels which can be inhibited by glibenclamide and may also involve additional relaxant mechanisms of action independent of K+ channel opening.抄録全体を表示PDF形式でダウンロード (457K) -
Masayuki Uchida, Shingo Yano, Kazuo Watanabe1991 年 57 巻 3 号 p. 377-385
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe effect of capsaicin-sensitive nerve degeneration (capsaicin-treatment) was investigated on the antral ulcer induction by the combined administration of 2-deoxy-D-glucose (2-DG; 200 mg/kg, i.v.), aspirin (200 mg/kg, p.o.) and 1% ammonia solution (10 ml/kg, p.o.) in male Sprague-Dawley rats. On the 2nd day after ulcer induction, erosive lesions were seen in the corpus, and ulcers penetrating into the muscularis mucosae were also seen in the antrum. In the capsaicin-treated rats, the antral ulcer was significantly aggravated as compared with that in capsaicin non-treated rats, although no difference was noted in the formation of corpus lesions between capsaicin-treated rats and non-treated rats. Acid output was investigated in pylorus ligated rats. 2-DG significantly increased the acid output. A significant increase in acid output was also observed in capsaicin-treated rats, and this increase tended to be augmented by the additional treatment with 2-DG. Atropine sulfate inhibited the significant increase in acid output of the capsaicin-treated rats. In all rats, both capsaicin-treated and pylorus-ligated, 2-DG induced antral ulcers that penetrated into the muscularis mucosae. From the above results, it was suggested that capsaicin-sensitive nerve degeneration modifies the gastroprotective ability in the antral mucosa to a greater extent than in the fundic mucosa, and this aggravation may be caused by activation of the vagus nerve, although the role of acid is not completely excluded.抄録全体を表示PDF形式でダウンロード (655K) -
Takeshi Kamato, Keiji Miyata, Hiroyuki Ito, Hidenobu Yuki, Mayumi Yama ...1991 年 57 巻 3 号 p. 387-395
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーYM060, (R)-5-[(1-methyl-3-indolyl)carbonyl]-4, 5, 6, 7-tetrahydro-1H-benzimidazole hydrochloride, is a new serotonin (5HT)3-receptor antagonist. We examined the effects of YM060 on chemotherapeutic agent-, apomorphine- and copper sulfate-induced emesis. Intravenous YM060 potently prevented cisplatin (10 mg/kg, i.v.)-induced emesis with ED50 values of 0.06 (0.05-0.07) μg/kg, i.v. in ferrets. Based on the ED50 values, YM060 was 300, 20 and 100 times more potent than ondansetron, granisetron and the S-isomer of YM060, respectively. The relative potencies of these drugs described above were similar to those in the previously reported 5HT3-receptor antagonism. YM060 given orally also potently inhibited cisplatin (10 mg/kg, i.p.)- and cyclophosphamide (200 mg/kg, i.p.)-induced emesis in ferrets with ED50 values of 0.1 (0.09-0.11) and 0.02 (0.16-0.27) μg/kg, p.o., respectively. All tested 5HT3-receptor antagonists including YM060 failed to prevent apomorphine (0.1 mg/kg, s.c.)-induced emesis in dogs and copper sulfate (1%, 10ml, p.o.)-induced emesis in ferrets. Our data indicate that YM060 is a highly potent inhibitor of chemotherapeutic agent-induced emesis and that the antiemetic effect of YM060 may be depend on 5HT3-receptor antagonism.抄録全体を表示PDF形式でダウンロード (440K) -
Ikuko Kimura, Mari Okazaki, Teruko Uwano, Shinjiro Kobayashi, Masayasu ...1991 年 57 巻 3 号 p. 397-403
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe effects of a depolarizing neuromuscular blocker on electrically evoked acetylcholine (ACh) release were studied using a mouse phrenic nerve-diaphragm muscle preparation preloaded with [3H]-choline, and the changes in muscle tension were recorded simultaneously. Succinylcholine at a low concentration (1 μM) enhanced evoked [3H]-ACh release, which tended to follow the increase in peak amplitude of tetanic tension; whereas at high concentrations (10 and 30 μM), it simultaneously reduced both release and tension. Decamethonium even at 10 and 30 μM had little effect on [3H]-ACh release despite producing a significantly greater reduction in tension compared with succinylcholine. (+)-Tubocurarine (5 μM) prevented the enhancing effect of [3H]-ACh release induced by 1 μM, but not the decreasing effect induced by 10 μM succinylcholine. These results suggest that succinylcholine induced acceleration at low concentrations due to a positive feedback mechanism through presynaptic nicotinic ACh receptors and the inhibition of ACh release at high concentration contributes in part to the neuromuscular blockade.抄録全体を表示PDF形式でダウンロード (365K) -
Kenji Takami, Tadatoshi Hashimoto, Akio Shino, Naohisa Fukuda1991 年 57 巻 3 号 p. 405-417
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーSpinal cord injuries in rats were experimentally produced by compressing the cord (T11 vertebra level) for 60 min with stainless steel screws. Morphometric analysis of the injured cord revealed that at 14 days post-injury, there were significant correlations between the neurologic score (NS) and all morphometric parameters, including total cross-sectional area (rs = 0.438), lesioned area (rs = -0.421) and area of the gray (rs = 0.377) and white matter (rs = 0.704). Although rats treated with thyrotropin-releasing hormone (TRH; 22.5 mg/kg, s.c., twice daily for 7 days starting 24 hr post-injury) showed significant improvement in NS 14 days post-injury, there were no significant differences in morphometric parameters between saline- and TRH-treated rats. In addition, no significant correlation was observed between NS and any of the morphometric parameters in TRH-treated rats, even though there was a significant correlation between the area of white matter and NS in saline-treated rats. These results suggest that neurologic recovery closely reflects the histopathological changes evident at the injury site in the present model, and that the improvement of neurologic status seen in rats with cord injury given TRH starting 24 hr post-injury is not due to protection against progression of neural damage at the injury site.抄録全体を表示PDF形式でダウンロード (1771K) -
Yasuo Oyama, Lumi Chikahisa, Fukiyo Tomiyoshi, Hiromi Hayashi1991 年 57 巻 3 号 p. 419-424
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーEffects of triphenyltin on mouse thymocytes were examined using fluorescent dyes to monitor membrane potential and intracellular Ca2+. Triphenyltin at 3 × 10-7 M to 1 × 10-6 M hyperpolarized thymocytes and depolarized them at 3 × 10-6 M or more, associated with increasing intracellular Ca2+. Hyperpolarization was suppressed by quinine, but not by tetraethylammonium and 4-aminopyridine, suggesting the involvement of Ca2+-activated K+ current. Triphentyltin failed to hyper-polarize thymocytes in Ca2+-free solution. Results indicate that triphenyltin promotes Ca2+-influx to thymocytes. Such an action of triphenyltin may be related to the immunotoxicity of organotins.抄録全体を表示PDF形式でダウンロード (320K) -
Hisashi Kuribara, Sakutaro Tadokoro1991 年 57 巻 3 号 p. 425-429
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーA noncompetitive NMDA antagonist MK-801 (0.03-0.3 mg/kg, i.p.) increased the response rate of mice trained under the discrete shuttle avoidance situation to a degree similar to the increase by methamphetamine (0.1-1 mg/kg, i.p.). The cholecystokinin-like decapeptide ceruletide significantly reduced the response-increasing effect of MK-801 (0.1 mg/kg) at 0.001 μg/kg; however, only 10 μg/kg of ceruletide, which per se inhibited the response, attenuated that of methamphetamine (0.3 mg/kg). The coadministration of MK-801 (0.1 mg/kg) and methamphetamine (0.3 mg/kg) produced no potentiation of the effect, and almost the same effect was maintained even after the additional administration of ceruletide (0.1 μg/kg).抄録全体を表示PDF形式でダウンロード (256K) -
Yoichiro Abe, Yoshitoshi Kasuya, Michiyo Kudo, Kamejiro Yamashita, Kat ...1991 年 57 巻 3 号 p. 431-435
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーEndothelin-1 (ET), a potent vasoconstrictor, induces a sustained increase in the phosphorylation level of the 20-kDa myosin light chain (MLC) in porcine coronary artery strips. ET also induces late phosphorylation of caldesmon, which is mimicked by 12-deoxyphorbol 13-isobutyrate, but not by 60 mM KCl. Nitroglycerin, a vasorelaxant, completely reverses the ET-induced phosphorylation of MLC, but not that of caldesmon. These results suggest an important regulatory role of MLC phosphorylation in ET-induced contraction.抄録全体を表示PDF形式でダウンロード (359K) -
Akio Fujimura, Tsuyoshi Shiga, Kyo-ichi Ohashi, Akio Ebihara1991 年 57 巻 3 号 p. 437-441
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーTrichlormethiazide was given orally to rats at 10 a.m. or 10 p.m. for 14 days. The diuretic effects of the agent at 10 a.m. were greater than those at 10 p.m. on day 14. Serum concentrations of triglyceride and glucose increased in both trials. The increments in these parameters were enhanced following trichlormethiazide at 10 a.m. These data indicate that the diuretic effects of trichlormethiazide and its untoward influences on serum metabolic parameters might vary with the administration time during a repeated therapy.抄録全体を表示PDF形式でダウンロード (217K) -
Shigeru Nakamura, Hiromu Kawasaki, Koichiro Takasaki1991 年 57 巻 3 号 p. 443-446
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーEffects of intracerebroventricular (i.c.v.) treatment with atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) on the pressor response to i.c.v.-injected clonidine were investigated in conscious rats. I.c.v.-pretreatment with ANP (10 μg) or BNP (10 μg) inhibited the pressor response to i.c.v.-injected clonidine (10 μg). Systemic (i.v.) treatment with ANP and BNP had no such effect. These results suggest that natriuretic peptides in the brain modulate the centrally mediated pressor response to clonidine.抄録全体を表示PDF形式でダウンロード (210K) -
Hisanori Takanashi, Zen Itoh1991 年 57 巻 3 号 p. 447-451
発行日: 1991年
公開日: 2006/07/11
ジャーナル フリーThe gastric antisecretory activity of 15(R)-15-methylprostaglandin E2 (arbaprostil) was compared with that of natural prostaglandin (PG) E2 in Pavlov pouch dogs. Arbaprostil significantly inhibited pentagastrin and food-stimulated gastric secretion when it was administered directly into the pouch at a dose of 10-30 μg/pouch and 30-300 μg/pouch, respectively. Natural PGE2, however, was inactive up to 1000 μg/pouch. The data indicate that arbaprostil is a potent, long-acting orally active antisecretory drug that may be useful for the treatment of peptic ulcer disease.抄録全体を表示PDF形式でダウンロード (252K)
- |<
- <
- 1
- >
- >|