The Japanese Journal of Pharmacology
Online ISSN : 1347-3506
Print ISSN : 0021-5198
ISSN-L : 0021-5198
Volume 57 , Issue 4
Showing 1-19 articles out of 19 articles from the selected issue
  • Tsutomu Suzuki, Kokichi Otani, Miwa Misawa
    1991 Volume 57 Issue 4 Pages 455-462
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    The purpose of this experiment is to investigate genetic differences in the development of physical dependence on morphine and codeine in inbred strains of mice, C57BL/6, C3H/He and DBA/2. Mice were treated with morphine- or codeine-admixed food (1, 2 and 3 mg/g of food) for 3 to 9 days. After the termination of drug treatment, the mice were given naloxone (5 mg/kg, s.c.). The incidences of jumping and teeth chattering by naloxone challenge in morphine and codeine-treated C57BL/6 mice were much greater than those in C3H/He and DBA/2 mice. However, the incidences of other naloxone-precipitated withdrawal signs, such as ptosis and diarrhea, were not different among the three inbred strains of mice. These results indicate that genotype is an important determinant of the degree of most naloxone-precipitated withdrawal signs in morphine- and codeine-treated mice.
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  • Hisakuni Hashimoto, Natsuki Satoh, Mitsuyoshi Nakashima
    1991 Volume 57 Issue 4 Pages 463-472
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Time-dependent inhibition of sodium channels by class I antiarrhythmic drugs has been observed in isolated cardiac muscles or cells. We examined coupling interval-related effects of class I antiarrhythmic drugs, mexiletine, cibenzoline and disopyramide, on ventricular activation in canine infarcted myocardium. A ventricular stimulation with various coupling intervals was applied to the right ventricle, and activation delays (time intervals between the initiation of a deflection and the final rapid deflection of a bipolar electrocardiogram) of infarcted and normal zones were measured. The premature stimulation produced a delayed activation and in some animals, caused reentrant beats. Mexiletine (3 and 10 mg/kg), cibenzoline (1 and 4 mg/kg) and disopyramide (1 and 4 mg/kg) further enhanced or blocked the delayed activation. The effects of these drugs were more marked at shorter coupling intervals, although cibenzoline and disopyramide showed significant effects also at long coupling intervals. The effect of these drugs on the activation in the normal zone was less than that in the infarcted zone. In conclusion, mexiletine, cibenzoline and disopyramide showed a coupling interval-related depression of delayed activation in infarcted myocardium, which may be a reflection of their time-dependent inhibition of sodium channels.
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  • Chiaki Kamei, Kenji Tasaka
    1991 Volume 57 Issue 4 Pages 473-482
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    The effects of intravenous and intracerebroventricular administrations of certain H1-blockers on the active avoidance response in rats were studied. Among the classic H1-blockers used in this study: pyrilamine, diphenhydramine, promethazine and chlorpheniramine, promethazine was the most effective and chlorpheniramine the least in inhibiting the active avoidance response; namely, a variation of prolongation in the response latency of the avoidance response. Meanwhile, ketotifen most potently inhibited the active avoidance response when the drugs were administered intracere-broventricularly. Mequitazine, astemizole and oxatomide were weak depressants when administered by either route. Azelastine was less effective than the classic H1-blockers by intravenous injection, while by intracerebroventricular injection, the inhibition was almost identical to those induced by the classic H1-blockers. Intracerebroventricular injection of histamine was antagonized the prolonged latency in the avoidance response induced by pyrilamine or diphenhydramine. A similar effect was also produced by 2-methylhistamine, but 4-methylhistamine had no effect. Intracerebroventricular injection of acetylcholine was restored the retarded avoidance response induced by pyrilamine, but a dose 20 times greater than that of histamine was required. From these findings, it can be concluded that inhibition of the active avoidance response induced by H1-blockers may be exerted through interaction with H1-receptors in the brain.
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  • Toshio Ohnuki, Yasuyuki Nomura
    1991 Volume 57 Issue 4 Pages 483-493
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Phosphatidylinositol (PI) turnover via muscarinic acetylcholine (mACh) receptor was investigated using the cerebral cortex from adult rats. Activities in the cerebral cortex, hippocampus and striatum from senescent rats were compared with those from adult rat. Carbachol (1 mM)-stimulated [3H]IP accumulation in the presence of 10 mM LiCl was inhibited by pirenzepine more potently than by AF-DX 116. Although the displacing activity of carbachol for [3H]pirenzepine binding was decreased by 50 μM GTPγS, pretreatment of slices with pertussis toxin (PTX, 0.01-1.0 μg/ml) did not affect the carbachol-induced [3H]IP accumulation. In the slices from all 3 tissues, cerebral cortex, hippocampus and striatum, both incorporation of [3H]inositol and carbachol-stimulated [3H]IP accumulation were reduced at 28 months compared to those at 2 months. Furthermore, the Bmax values of [3H]pirenzepine binding in membranes from these three regions were diminished at the senescent stage. Taken together, the results suggest that an M1-subtype of muscarinic acetylcholine receptor could be involved in PI turnover via GTP-binding proteins insensitive to PTX. Age-related changes in M1-receptor mediated PI turnover seem to be in part due to the decreased number of M1-receptors with increasing age in the cerebral cortex, hippocampus and striatum; and some qualitative changes also seem to have occurred in the hippocampus of senescent rats in the mACh receptor-PI turnover system.
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  • Yasuo Morimoto, Koichi Shimohara, Shinya Oshima, Takayuki Sukamoto
    1991 Volume 57 Issue 4 Pages 495-505
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Effects of KB-5492, a new anti-ulcer agent, on various experimental gastric mucosal lesions and mucosal defensive factors in rats were compared with those of teprenone and cimetidine. KB-5492 administered orally at 12.5-200 mg/kg inhibited water-immersion stress- and indomethacin-induced gastric mucosal lesions in a dose-dependent manner with ED50 values of 46 and 27 mg/kg, respectively, indicating that KB-5492 was more potent than teprenone but less potent than cimetidine. KB-5492, administered orally at 12.5-100 mg/kg, also inhibited ethanol-induced gastric mucosal lesions in a dose-dependent manner with an ED50 of 23 mg/kg, so KB-5492 was 3 times more potent than teprenone, whereas cimetidine produced no obvious inhibition. In addition, KB-5492, administered orally at 25 and 50 mg/kg twice daily for 10 consecutive days, significantly accelerated the healing of acetic acid-induced gastric ulcers more potently than teprenone and cimetidine. KB-5492 at anti-ulcer doses significantly increased gastric mucosal blood flow in normal anesthetized rats and inhibited the reduction of gastric mucosal hexosamine content induced by aspirin, but did not affect gastric acid secretion in pylorus-ligated rats. These results indicate that KB-5492 has potent and broad anti-ulcer properties, which are probably exerted by its enhancement of gastric mucosal defensive factors through increasing gastric mucosal blood flow and/or retaining gastric mucus, and not by its inhibition of gastric acid secretion.
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  • Ken Nakazawa, Tomokazu Watano, Mica Ohara-Imaizumi, Kazuhide Inoue, Ka ...
    1991 Volume 57 Issue 4 Pages 507-515
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Effects of hirsutine, an alkaloid that produces a potent ganglion blocking effect, were investigated using rat pheochromocytoma PC12 cells. Hirsutine (1 to 10 μM) suppressed dopamine-release evoked by 100 μM nicotine. In voltage-clamped cells, hirsutine (1 to 10 μM) inhibited the inward current activated by 100 μM nicotine. Hirsutine was equipotent to hexamethonium in blocking the nicotine-activated current. The voltage-dependency of the nicotine activated current was not modified by hirsutine. Effects of hirustine on other ion channels were tested to determire its selectivity. Inward currents mediated through ATP-activated channels were scarcely affected by hirsutine (up to 100 μM). However, hirustine (10 μM) inhibited Ba currents passing through Ca channels and K currents activated by depolarizing voltage steps. The results suggest that hirsutine potently blocks nicotinic receptor-channels, but hirsutine also inhibits voltage-gated Ca and K channels. Roles of the inhibition of these channels in the pharmacological effects of hirsutine were discussed.
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  • Masami Kubo, Takashi Ochiai, Jyouji Kato, Ryuichi Ishida
    1991 Volume 57 Issue 4 Pages 517-526
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    The long-term oral administration of TA-6366 (5 mg/kg/day) from 4-weeks old impeded the genetic hypertension development with only a slight decrease in heart rate in spontaneously hypertensive rats (SHRs). However, the lower dose (1 mg/kg/day) of TA-6366 did not affect the development, but it lowered blood pressure after the development was almost accomplished. Concomitantly, relative heart weights in both the groups were markedly decreased to almost the same degree. The reduction of ACE activity in the aorta, brain and lung of both groups was found at 24 hr after the final administration, particularly at the 5 mg/kg/day dose; and that of the aorta was kept at almost the same low level even on the 9th day after withdrawal. After withdrawal of TA-6366 (5 mg/kg/day), the significant decrease in blood pressure was sustained at least for 10 weeks. The beneficial effect of TA-6366 on the hypertension development in SHRs seems to be related to its strong and long-lasting ACE inhibition, especially in the vasculature.
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  • Noboru Toda, Yuji Tanobe, Hiroshi Baba
    1991 Volume 57 Issue 4 Pages 527-534
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    In dog duodenal longitudinal muscle strips, transmural electrical stimulation (10 Hz, 15 sec) elicited a transient contraction, which was abolished by tetrodotoxin and atropine but potentiated by treatment with NG-nitro-L-arginine (L-NA), a nitric oxide (NO) synthesis inhibitor. The potentiation was reversed by L-arginine but not by its D-enanthiomer. Acetylcholine-induced contractions were not influenced by L-NA. After treatment with atropine, the electrical neural stimulation relaxed the muscle strips partially contracted with bradykinin, the relaxation being abolished by tetrodotoxin and suppressed by L-, but not D-, NA. L-arginine reversed the L-NA-induced inhibition. Oxyhemoglobin abolished the relaxation caused by nerve stimulation and NO. The neurally-induced relaxation was not attenuated by adrenoceptor antagonists and indomethacin. It is concluded that electrical stimulation of non-adrenergic, non-cholinergic nerves relaxes dog duodenal smooth muscle, due possibly to NO produced upon neural excitation, and potentiation by L-NA of the contractile response to cholinergic nerve stimulation would be derived from elimination of the neurally-induced relaxation.
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  • Ikunobu Muramatsu, Shigeru Kigoshi, Tsuyoshi Ohmura
    1991 Volume 57 Issue 4 Pages 535-544
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    We tried to determine α1-adrenoceptor subtypes involved in noradrenaline-induced contractions of rat thoracic aorta and dog carotid artery. Prazosin competitively antagonized the contractions induced by noradrenaline in both the arteries with a high pKB value (approximately 9.7). WB4101, benoxathian, phentolamine, HV723 and 5-methylurapidil also competitively antagonized the responses to noradrenaline in both the arteries: however, the affinities for the antagonists were significantly higher in the rat thoracic aorta than in the dog carotid artery. The affinities for the competitive antagonists were not changed by treatment with nifedipine. In the rat thoracic aorta, chlorethylclonidine (CEC) elicited either a persistent contraction with rhythmic activities before treatment with nifedipine or partial inactivation of α1-adrenoceptors in the presence of nifedipine. On the other hand, CEC produced only inactivation of α1-adrenoceptors in the dog carotid artery. These results suggest that noradrenaline-induced contractions of the rat thoracic aorta and dog carotid artery are respectively mediated through distinct α1-adrenoceptor subtypes. According to the α1A, α1B subclassification, the α1-adrenoceptor of dog carotid artery is like the α1B subtype, while that of rat thoracic aorta is atypical. Both subtypes are also identified as a high affinity site for prazosin (α1H subtype) in the α1H, α1L and α1N subclassification.
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  • Jun Kojima, Yoshiko Sugawara, Shosaku Obara
    1991 Volume 57 Issue 4 Pages 545-552
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    NIK-247 (9-amino-2, 3, 5, 6, 7, 8-hexahydro-1H-cyclopenta[b]-quinoline hydrochloride hydrate), an acetylcholinesterase inhibitor, is structurally related to 4-aminopyridine (AP). Its effects on ionic currents were examined in the artificial node of the crayfish axon under voltage-clamp. When applied externally, NIK-247 reversibly suppressed both inward and outward currents. Effects on K currents were further studied in the presence of tetrodotoxin. NIK-247 suppressed the K current dose-dependently, but with an IC50 at of 10-3 M. THA (9-amino-1, 2, 3, 4-tetra-hydroacridine hydrochloride hydrate), a related inhibitor, similarly suppressed the K current with an IC50 of 5 × 10-4 M, in comparison with 3-AP and 4-AP which had IC50's of 3 × 10-5 M and at 10-5 M, respectively. Furthermore, NIK-247 (and THA) suppressed the K current uniformly for the whole time course, whereas AP the AP's suppressed mainly the fast activating and inactivating K current with a voltage- and frequency-dependent recovery. Therefore, NIK-247 and THA seem to be neither potent nor very specific as ionic channel blockers. With respect to the K current, however, they clearly differ from the AP's in their mode of suppression.
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  • Hitoshi Houchi, Mami Azuma, Motoo Oka, Kyoji Morita
    1991 Volume 57 Issue 4 Pages 553-558
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    The effect of idebenone, an agent improving cerebral metabolism, on catecholamine secretion was examined using primary cultures of bovine adrenal chromaffin cells. Catecholamine secretion evoked by acetylcholine was markedly inhibited by idebenone, and this effect was concentration-dependent. In contrast, other cerebral metabolism-improving agents, such as hopantenate and prope ntofylline, failed to cause any significant effect on the secretion in the same concentration range. Further more, idebenone inhibited the secretion evoked by high K+, veratridine, and Ba2+, but failed to inhibit the secretion evoked by the Ca2+-ionophore A23187. Idebenone also inhibited the radioactive Ca2+ uptake stimulated by acetylcholine or high K+ under the conditions in which its inhibitory action on the secretion was observed. Nifedipine, a typical voltage-dependent Ca2+ channel blocker, inhibited the secretion evoked by high K+, and this inhibitory action on the secretion was markedly reduced by the presence of idebenone. The present results suggest that idebenone may inhibit the influx of extracellular Ca2+ into the cells presumably through its blocking action on the voltage-dependent Ca2+ channels, resulting in the inhibition of catecholamine secretion in the adrenal chromaffin cell.
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  • Hisanori Takanashi, Yoshiki Kawabe, Michitaka Akima
    1991 Volume 57 Issue 4 Pages 559-564
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Gastric acid antisecretory activities of 15(R)-15-methylprostaglandin E2 (arbaprostil) preincubated or not preincubated with 0.9% physiological saline, the pH of which was precisely adjusted to less than 4.30, were examined in pylorus-ligated rats, and compared with those of 15(S)-15-methylprostaglandin E2 (15(S), epimer of arbaprostil). 15(S), unlike arbaprostil without preincubation, when s.c.-administered to rats significantly inhibited gastric acid secretion in a dose-dependent manner (30-300 μg/kg). However, arbaprostil preincubated at 37°C for 30 min with 0.9% saline, at pHs of 4.30, 2.75 and 1.20, respectively, showed the following order of pH-dependent antisecretory activities: 1.20 > 2.75 > 4.30. An increase in 15(S) formation from arbaprostil in a pH-dependent manner was also observed by radioisotopic experiments under the same incubation conditions using [3H]-labeled arbaprostil. The present result suggests that the gastric antisecretory effect of arbaprostil can be mainly explained in terms of the formation of 15(S) after oral administration.
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  • Akio Fujimura, Kyo-ichi Ohashi, Akio Ebihara
    1991 Volume 57 Issue 4 Pages 565-569
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    The present study was undertaken to examine whether urinary excretions of prostaglandins increase by repeated administration of a non-toxic dose of lithium. Our previous study demonstrated that 2 mEq/kg/day of lithium chloride (LiCl) is not a toxic dose; and therefore, this dose of LiCl in 1 ml vehicle (5% glucose solution) or 1 ml of vehicle alone was injected intraperitoneally for 7 days into Wistar rats. On day 7, 3% body weight of 1% NaCl solution was given orally; and urine for the determination of PGE2 and 6-keto-PGF, a metabolite of PGI2, was collected for 6 hr after dosage. Thereafter, blood samples for measuring plasma renin activity (PRA) were obtained. The urinary amounts of PGE2 and 6-keto-PGF in the Litreated rats were significantly greater than those in the control animals. The values of PRA did not significantly differ between the two groups of rats. These findings indicate that the production of prostaglandins, including those of PGE2 and PGI2, are enhanced during repeated administration of a non-toxic dose of lithium. The enhanced production of prostaglandins might not be mediated through the activated renin-angiotensin system.
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  • Hiroko Miyagi, Makie Higuchi, Michio Nakayama, Hidehiko Moromizato, Ma ...
    1991 Volume 57 Issue 4 Pages 571-581
    Published: 1991
    Released: July 11, 2006
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    To estimate the participation of a Na+, K+-ATPase-inhibiting plasma foctor in pregnancy induced hypertension (PIH), the inhibitory activity and the characteristics of plasma extract eluted with ethanol through a C8 column were examined in normotensive non-pregnant women (N) and women with normal pregnancy (NP) and PIH. There were no differences among the 3 groups in the Na+, K+-ATPase activity of erythrocyte ghosts. The heat- and acid-stable plasma extract dose-dependently inhibited Na+, K+-ATPase activity with a pattern similar to that of ouabain, but different from that of vanadate. The inhibitory activity of plasma extract was not influenced by polyclonal digoxin antibody which almost completely prevented digoxin-induced inhibition and slightly but significantly reduced the ouabain-induced one. The results indicate that the plasma extract has ouabain-like inhibitory activity on Na+, K+-ATPase and that it is not endogenously synthesized digoxin itself, but a substance differing in structure from digoxin. Furthermore, the ouabain-like Na+, K+-ATPase inhibitory activity in NP plasma was significantly lower than that in PIH plasma, which was similar to that in N plasma. There were significant relationships between the ouabain-like Na+, K+-ATPase inhibitory activities in plasma and the diastolic and systolic blood pressures in NP and PIH groups. The results suggest that the lower ouabain-like Na+, K+-ATPase inhibitory activity in plasma probably participates in maintaining the blood pressure within the normal range during pregnancy and its failure may be involved in the genesis of PIH.
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  • Hirohiko Akamatsu, Yoshiki Miyachi, Yasuo Asada, Yukie Niwa
    1991 Volume 57 Issue 4 Pages 583-589
    Published: 1991
    Released: July 11, 2006
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    The effects of azelastine, an orally active anti-allergic drug, on several inflammatory parameters of human neutrophils, including human neutrophil chemotaxis, phagocytosis and generation of reactive oxygen species (ROS), was examined. ROS generated in a cell-free, xanthine-xanthine oxidase system was also assessed. The species investigated were superoxide radical anion (O2-), hydrogen peroxide (H2O2) and hydroxyl radical (OH·). Azelastine significantly inhibited human neutrophil phagocytosis and the generation of O2-, H2O2, OH· by human neutrophils. However, the drug did not markedly affect human neutrophil chemotaxis or the ROS levels generated in the xanthine-xanthine oxidase system. The present study indicates that azelastine may exert an anti-inflammatory action by inhibiting human neutrophil phagocytosis as well as oxygen radical generation at the sites of inflammation.
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  • Shinjiro Nakajyo, Tatsunori Fukui, Yutaka Hara, Kazumasa Shimizu, Nori ...
    1991 Volume 57 Issue 4 Pages 591-600
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Tiamulin with an IC50 of 1.7 × 10-6 M inhibited both the rapid and sustained contractions induced by hyperosmotically added 60 mM K+ (Hyper 60 K+) without changing the membrane potential in the intestinal muscle. Tiamulin inhibition (2 × 10-6-2 × 10-5 M) of the Ca2+-induced contraction in depolarized muscle was competitively antagonized by raising external Ca2+. Tiamulin (2 × 10-5 M) slightly affected the Hyper 60 K+-induced phasic contraction under hypoxia and the carbachol-induced phasic contraction. Moreover, tiamulin (2 × 10-5 M) inhibited the Hyper 60 K+-induced contraction with decreasing [Ca2+]cyt level. Although the inhibitory effect of 10-7-10-5 M monesin, an inhibitor of mitochondrial respiration, on the Hyper 60 K+-induced contraction was reduced under hypoxia, the effect of tiamulin (2 × 10-7-2 × 10-4 M) was not modified. Tiamulin changed neither the intracellular Na+ and K+ content of the depolarized muscle nor the Ca2+-induced contraction in the chemically skinned preparations. These results suggest that the inhibitory action of tiamulin on the Hyper 60 K+-induced tonic contraction is possibly due to the competitive inhibition of Ca2+ entry through the voltage-dependent Ca2+ channel of the intestinal smooth muscle cell.
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  • Lisa Imamura, Hiroyuki Ohta, Xiao-Hu Ni, Kinzo Matsumoto, Hiroshi Wata ...
    1991 Volume 57 Issue 4 Pages 601-608
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    To examine the working memory performance, gerbils were tested in the delayed nonmatching to position task using a T-maze, and the effects of cerebral ischemia on the performance were examined. There were no significant differences between gerbils and rats in the alternation performance without delay and with the interrun intervals ranging from 10 to 810 sec. These data suggest that this task is useful for assessing working memory in gerbils as well as in rats. Scopolamine (0.1 and 0.2 mg/kg) impaired the working memory performance in both species. Bilateral occlusion of the common carotid arteries for 5 min severely impaired the choice accuracy in the gerbils 1 to 3 days after the operation. This memory impairment was observed even at the shortest interval. One month after the operation, partial behavioral recovery was observed in the ischemic gerbils, in spite of a marked loss of the pyramidal cells in the hippocampus CA1 sector. These data indicate that the working memory performance is highly vulnerable to the cerebral ischemia and that the ischemic operation transiently but severely impairs the acquisition process of the working memory in gerbils.
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  • Hisanobu Shimaji, Hiroaki Shirahase, Shigeyoshi Morishita, Seimei Osum ...
    1991 Volume 57 Issue 4 Pages 609-612
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    The effects of indapamide (a nonthiazide antihypertensive diuretic) on the growth promoting activity of serum, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) or Ca3(PO4)2 on Balb/C 3T3 cells were studied. Indapamide inhibited the growth promoting activity of serum, but furosemide (a nonthiazide antihypertensive diuretic) had no such inhibitory effect. Indapamide inhibited the growth promoting activity of PDGF, but not that of FGF and Ca3(PO4)2. The present experiments demonstrate that indapamide selectively inhibits the growth promoting activity of PDGF.
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  • Lei-Ming Ren, Yasuyuki Furukawa, Yasuyuki Karasawa, Makoto Murakami, S ...
    1991 Volume 57 Issue 4 Pages 613-616
    Published: 1991
    Released: July 11, 2006
    JOURNALS FREE ACCESS
    Using an isolated, blood-perfused canine atrial preparation, we investigated the effects of omega-conotoxin GVIA (omega-CgTX), a blocker of N-type voltage-operated calcium channels, on the atrial contractile force and sinus rate. Omega-CgTX in a dose range of 0.3-3 nmol gradually attenuated the atrial contractile force in a dose-dependent manner, but did not affect the sinus rate, indicating that it can depress contractility but not pacemaker activity.
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