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Volume 51 (1989)
- Issue 4 Pages 455-
- Issue 3 Pages 309-
- Issue 2 Pages 151-
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Volume 51, Issue 2
Displaying 1-20 of 20 articles from this issue
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Shahin SANJAR, Diana SMITH, Elizabeth SCHAEUBLIN, Anne KRISTERSSON, Ia ...1989 Volume 51 Issue 2 Pages 151-160
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSIntravenous injection of platelet activating factor (PAF) in anesthetized guinea pigs induces non-selective airway hyperreactivity. This response to PAF was reduced in a dose-dependent manner by systemic administration of established prophylactic anti-asthma drugs (ketotifen, cromoglycate, aminophylline and glucocorticosteroids) and by competitive antagonists of PAF. These inhibitory effects could not be accounted for by antagonism of histamine (H1), serotonin or peptidoleukotrienes receptors; parasympatholytic activity; cyclo-oxygenase or lipoxygenase inhibition; mast cell stabilization; or bronchodilatation. Infusion or injection of PAF to induce airway hyperreactivity in the guinea pig may provide a prospective test for prophylactic anti-asthma drugs.View full abstractDownload PDF (556K) -
Diana SMITH, Shahin SANJAR, John MORLEY1989 Volume 51 Issue 2 Pages 161-166
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSIntravenous infusion of platelet activating factor (PAF) causes an accumulation of platelets within the thorax of the guinea pig that is accompanied by increased sensitivity of the airways to spasmogens. A crystal scintillation detector has been used for measurement of intrathoracic accumulation of 111Indium-labeled platelets during responses to PAF. PAF-antagonists inhibit both development of airway hyperreactivity and the accumulation of 111Indium-labeled platelets. Prophylactic anti-asthma drugs, which are known to inhibit development of airway hyperreactivity, do not diminish platelet accumulation in response to an intravenous infusion of PAF. It is therefore concluded that intrathoracic platelet accumulation per se is not the determinant of increased airway reactivity.View full abstractDownload PDF (314K) -
Shahin SANJAR, Sakai AOKI, Karima BOUBEKEUR, Lisa BURROWS, Ian COLDITZ ...1989 Volume 51 Issue 2 Pages 167-172
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSIntraperitoneal(i.p.) injection of platelet activating factor (PAF) in guinea pigs caused a dose-related increase in the number of eosinophils recovered from bronchoalveolar lavage fluid (BALF). The prevalence of eosinophils in BALF had significantly increased within 1 hr of i.p. injection of PAF (10 μg/animal) and was maximal after 24 hr. Subcutaneous osmotic mini-pumps were used to administer drugs for 5 days prior to i.p. injection of PAF (10 μg/animal) and for the subsequent 24 hr. The percentage increase of eosinophils in BALF, due to PAF, was inhibited in animals treated with dexamethasone, aminophylline, cromoglycate, tranilast or ketotifen, but not in animals treated with oxatomide, azelastine, amlexanox, ibudilast or AA-861. These results suggest that inhibition of pulmonary eosinophilia may be a necessary property of prophylactic anti-asthma drugs and provide indirect evidence favoring a role for PAF in eosinophilia of asthma.View full abstractDownload PDF (317K) -
Kazuo NAKAGAWA1989 Volume 51 Issue 2 Pages 173-179
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSHepatic glutathione content decreased in a dose-dependent manner after the administration of lead acetate (5-100 mg/kg, i.p.). Hepatic cysteine content, a substantial rate limiting factor in glutathione synthesis, also decreased transiently but significantly, whereas total cysteine (cysteine plus cystine) content remained unchanged. The pretreatment of mice with L-methionine (250 mg/kg, i.p.) partially prevented the decrease in glutathione content in lead-treated mice at least partly through the elevation of hepatic cysteine content; in contrast, L-cysteine administration (250 mg/kg, i.p.) depleted hepatic glutathione contrary to a quick increase in hepatic cysteine content. The activity of γ-glutamylcysteine synthetase (GCS), a rate limiting enzyme in glutathione synthesis, was not altered by either the administration of lead or sulfur amino acids. On the other hand, lead facilitated the disappearance of glutathione from the livers of mice treated with buthionine sulfoximine, a specific inhibitor of GCS. These lines of evidence suggest that for the decrease in glutathione content elicited by lead-loading, the increased efflux of glutathione into extra-hepatic spaces is a more crucial event than the fluctuation of intrahepatic cysteine concentration.View full abstractDownload PDF (378K) -
Yoshihiro SUZUKI, Jun-ichi SUDO1989 Volume 51 Issue 2 Pages 181-189
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSTo elucidate the nephrotoxic mechanisms of cephaloridine (CER), changes in renal contents of glutathione (GSH), glutathione disulfide (GSSG), reduced and oxidized nicotinamide adenine dinucleotide phosphates (NADPH and NADP) and changes in renal activities of glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase were examined for 15 days in rats that received single intravenous injections of CER in doses of 0 (control), 100 and 1, 000 mg/kg body weight. Significantly different changes from the control group were observed in the 1, 000 mg/kg group. The 1, 000 mg/kg group showed elevations in renal NADP and NADPH contents and decrements in renal GSH content in the period of the 1 st to 3rd hour after the CFR-administration. Thus, the fall in renal GSH content was considered to be a cause for renal injury due to the oxygen radicals observed in the early period. After the 6th hour, the 1, 000 mg/kg group showed decreases of renal glutathione peroxidase and glutathione reductase activities and increases of renal glucose-6-phosphate dehydrogenase activity as well as GSH content. Although accumulation of GSH in the kidney was clearly observed in the late period, the more highly aggravated renal injury was speculated to be due to the decreased level in the utilization of GSH according to the fall of renal glutathione peroxidase activity.View full abstractDownload PDF (508K) -
Hiroichi NAGAI, Motonori AOKI, Tsukasa SHIMAZAWA, Ikuhisa YAKUO, Akihi ...1989 Volume 51 Issue 2 Pages 191-197
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe effects of OKY-046, a selective thromboxane A2 (TXA2) synthetase inhibitor, and ONO-3708, a novel TXA2 receptor antagonist, on liver disease were investigated in mice. The liver injury was induced by either an injection of antibasic liver protein (BLP) antibody into DBA/2 mice that had been previously immunized with rabbit lgG or by an injection of bacterial lipopolysaccharide (LPS) into Corynebacterium parvum (C. parvum) pretreated DDY mice. 1) In both injury models, clear elevation of glutamate transaminase (GOT and GPT) activity due to extensive liver parenchymal cell damage was observed; this was confirmed by significant histopathological changes in the liver. 2) Typical histopathological changes in the liver were submassive hepatocellular necrosis in the anti-BLP antibody-induced injury model and focal necrosis in the LPS-induced model. Inflammation and increased cell infiltration in portal connective tissue were observed in both cases. 3) Administration of OKY-046 (50 mg/kg) and ONO-3708 (0.5, 1.0 and 2.0 mg/kg) suppressed the elevation of serum GOT and GPT levels and histopathological changes in both experimental liver injury models. 4) Indomethacin inhibited the development of liver disease caused by anti-BLP antibody but not by bacterial LPS. Prostaglandin I2 inhibited the elevation of serum GOT and GPT levels and histopathological changes of the liver in the mice treated with anti-BLP antibody and showed the tendency to inhibit the development of liver injury caused by bacterial LPS.View full abstractDownload PDF (402K) -
Mario GALCIA-ALVES, Yoshihiro KADOWAKI, Yuji IWASHITA, Katsuhide NISHI1989 Volume 51 Issue 2 Pages 199-209
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of a newly introduced polyoxyethylene-modified superoxide dismutase (SOD-POE) on reperfusion induced arrhythmias were examined in the pentobarbital anesthetized rat. Reperfusion induced arrhythmias were elicited by occlusion of the left anterior descending coronary artery (LAD) for 15 min and subsequent release. The LAD occlusion was performed by compressing the artery using a suction cup of 2 mm in diameter placed on the LAD to which negative pressure was applied. The LAD occlusion and release was repeated at an interval of 30 min. SOD-POE or human SOD (h-SOD) (1000 U/kg) was injected intravenously 1 5 min prior to the occlusion at the second trial of the occlusion. In the control group, various types of arrhythmias including ventricular fibrillation (Vf), ventricular tachycardia (VT), premature ventricular contraction (PVC) and premature atrial contraction (PAC) were elicited immediately after release of the occlusion. In the SOD-POE-treated group, Vf and VT were completely prevented and the numbers of PVC and PAC significantly decreased, while pretreatment with h-SOD did not prevent the occurrence of reperfusion induced arrhythmias. The protective effects of SOD-POE lasted for more than 90-120 min. The plasma half life for SOD-POE was 10.8 hr, while that for h-SOD was 8.6 min. Results indicate that intravenous administration of SOD-POE would provide a new means of preventing reperfusion induced arrhythmias occurring in clinical situations.View full abstractDownload PDF (610K) -
Toru EGASHIRA, Takayuki NAGAI, Yoshihira KIMBA, Ritsuko TAKANO, Yasumi ...1989 Volume 51 Issue 2 Pages 211-218
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe effects of bifemelane hydrochloride (BF) upon various cholinergic markers, muscarinic receptors, acetylcholinesterase (AChE) and choline acetyltransferase (CAT), in the aged rat brain were examined. Marked reduction of the density of muscarinic receptors (Bmax) as well as AChE and CAT activity concomitant with aging was observed. Administration of BF in daily doses of 10 mg/kg for 4 weeks to aged rats significantly decreased the apparent dissociation constant (Kd) for QNB in muscarinic receptors in the forebrain, but did not affect the value of Bmax. CAT activity also increased significantly compared with that of control aged rats, but administration of BF did not alter AChE activity. These results indicate that long-term treatment with BF enhances the affinity of muscarinic receptors for QNB as well as CAT activity and that BF may have therapeutic application in the treatment of CNS cholinergic dysfunctions.View full abstractDownload PDF (440K) -
Kikuo MASUDA, Akira SUZUKI, Takaaki NAKAMURA, Shoji TAKAGAKI, Kosei NO ...1989 Volume 51 Issue 2 Pages 219-226
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSOur previous studies showed that a new, substituted dihydrobenzoxazine, FK973 (11 -acetyl-8-carbamoyloxymethyl-4-formyl-14-oxa-1, 11-diazatetracyclo[7.4.1.O2, 7.O10, 12]tetradeca-2, 4, 6-trien-6, 9-diyl diacetate), which is a triacetylated derivative of the fermentation product FR900482 of Streptomyces sandaensis No. 6897, had potent antitumor effects on experimental tumors in vivo and in vitro. In the present study, we investigated the metabolism of FK973 in the blood of human and animals and the antitumor effects of its metabolites. After the incubation of FK973 in the blood (hemolysate) or serum of humans, dogs, rats and mice, it was rapidly metabolized to two diacetates and a monoacetate, and slowly to FR900482. FK973 and all its deacetylated metabolites showed strong cytotoxicity on in vitro cultured murine L1210 leukemia cells, and the cytotoxicity of FK973 was the most potent. In the in vivo experiments, FK973 and its metabolites prolonged the life of mice bearing ascitic P388 leukemia, and it potently inhibited the growth of murine B16 melanoma and Colon 38 adenocarcinoma implanted subcutaneously in mice. FK973 was the most effective compound. Thus, these results suggest that the antitumor effects of FK973 are stronger than those of its deacetylated metabolites produced in the blood of humans and animals.View full abstractDownload PDF (400K) -
Mitsuyoshi NINOMIYA, Tomoko TANI, Shigeyuki NAKAJIMA, Motohiko UEDA1989 Volume 51 Issue 2 Pages 227-238
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSS-312, a new calcium antagonist with a bicyclic dihydrothienopyridine structure, potently relaxed the helical strips of various isolated rabbit arteries precontracted with high K+-depolarization, serotonin (5-HT) and U46619 (thromboxane A2 analogue), and it competitively inhibited Ca++-induced contractions in depolarized basilar and femoral arteries. These effects of S-312 were more potent than nifedipine and almost comparable to or slightly more potent than those of nicardipine. In comparison with nifedipine and nicardipine, the calcium antagonistic effect and the relaxant effect on 5-HT-induced contractions of S-312 were most prominent in the basilar artery. The potent vasodilating action of S-312 in the high K+-depolarized basilar artery was not easily reversed by washing. S-312 did not affect Ca++-Induced contraction in the skinned fiber of guinea pig taenia caecum. The negative inotropic effect of S-312 in isolated guinea pig left atria was much less potent than those of nifedipine and nicardipine. S-312 above 10-7 M preferentially increased AV nodal conduction time in Langendorff-perfused isolated rabbit hearts; and above 3×10-8 M, it mainly decreased the maximum upstroke velocity of the action potential in isolated rabbit sinus node preparations. In summary, the present results indicate that S-312 is a potent new calcium antagonist possessing vasculoselectivity, especially for cerebral vessels.View full abstractDownload PDF (712K) -
Atsushi SUGIYAMA, Keitaro HASHIMOTO1989 Volume 51 Issue 2 Pages 239-246
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSCardiac effects of drugs used for circulatory disorders in traditional Japanese medicine based on ancient Chinese medicine (Kampo Medicine): Saikoka-ryukotsu-borei-to, Oren-gedoku-to, Toki-shakuyaku-san, Shimbu-to, Moku-boi-to, Ryo-kei-jutsu-kan-to, Sha-kanzo-to, Keishi-ninjin-to, Toki-to and Ryo-kan-kyo-mi-shin-ge-nin-to were investigated using canine isolated, blood-perfused sinoatrial node and papillary muscle preparations. Single injections of small doses of Oren-gedoku-to, Moku-boi-to and Ryo-kan-kyo-mi-shin-ge-nin-to (0.1 to 3 mg) dosedependently increased the sinoatrial rate and the developed tension of papillary muscle, while other drugs showed almost no effect on these parameters. All the drugs had almost no effect on the blood flow through the nutrient arteries of each preparation. The positive chronotropic and inotropic effects induced by Oren-gedoku-to, Moku-boi-to and Ryo-kan-kyo-mi-shin-ge-nin-to did not show tachyphylaxis and were not affected after pharmacological denervation by tetrodotoxin treatment or by reserpine pretreatment, but were significantly suppressed by atenolol. These results indicate that these three drugs act as beta-adrenoceptor agonists to produce clinically useful cardiac effects.View full abstractDownload PDF (342K) -
Rie MIYOSHI, Shozo KITO, Masanori SHIMOYAMA1989 Volume 51 Issue 2 Pages 247-255
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe distribution of muscarinic acetylcholine receptors (mAChR) was investigated in the monkey brain by means of quantitative in vitro autoradiography. 3H-QNB, 3H-pirenzepine (PZ) and 3H-AF-DX 116 were used for labelling total mAChR, M1 and M2 receptors, respectively. 3H-PZ and 3H-AF-DX 116 showed specificity to each receptor subtype in the monkey brain. On sections containing the putamen and giobus pallidus, the sum of Bmax values of 3H-PZ and 3H-AF-DX 116 binding sites was almost close to that of 3H-QNB binding sites. Autoradiographic distributions of muscarinic subtype receptors in the monkey brain were similar to those reported in the rat brain; that is, M1 receptors were dominant in most areas of the telencephalon, while M2 receptors were richly distributed in the brainstem and cerebellum. However, some nuclei of the brainstem such as the central gray matter, superior colliculus, substantia nigra, nucleus of the oculomotor nerve, pontine nucleus and inferior olivary nucleus, had relatively high ratios of M1 receptors in the monkey brain. In addition, the cortical lamminar distribution of M2 receptors noticed in the rat was not observed in the monkey brain. Knowledge about the localizations of M1 and M2 receptors in various brain regions in the monkey brain will increase our understanding of the functions of the brain cholinergic system in the primate.View full abstractDownload PDF (509K) -
Shiro MORIMOTO, Tadashi OHYAMA, Kazuhiro HISAKI, Yasuo MATSUMURA1989 Volume 51 Issue 2 Pages 257-265
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSRenal effects of CV-4093, a newly developed dihydropyridine calcium channel blocker, were examined using anesthetized stroke-prone spontaneously hypertensive rats, and the findings were compared with those of nicardipine. An intravenous injection of CV-4093 (2 μg/kg) produced long-lasting hypotension with a slow-onset accompanied by moderate renal vasodilation. There were no appreciable alterations in glomerular filtration rate (GFR) and urine formation, except that urine flow (UF) increased significantly during the first 10 min after injection. When CV-4093 was administered at 10 μg/kg, the hypotensive action was markedly augmented. Eighty minutes after the injection, a decrease in mean arterial pressure of about 45 mmHg was observed. Simultaneously, renal blood flow increased significantly from the control value of 5.76±0.46 ml/g·min to 6.94±0.28 ml/g·min. Renal vascular resistance decreased immediately after the injection, and the response lasted for over 3 hr, thereby indicating the marked and sustained renal vasodilating effect of CV-4093. GFR was constant throughout the experiment, but UF and urinary excretion of sodium were increased significantly. Fractional excretion of sodium was also elevated, thereby suggesting an inhibitory action of CV-4093 on renal tubular reabsorption of sodium. Nicardipine at a dose of 10, μg/kg, a dose producing an effective hypotensive action, caused no significant increases in RBF and urine formation. The renal vasodilating and diuretic actions of CV-4093 may provide a beneficial effect in the treatment of hypertension.View full abstractDownload PDF (407K) -
Eiji ITOH, Taeko HATA1989 Volume 51 Issue 2 Pages 267-272
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSNeurotropin, a nonprotein component extracted from the skin of rabbits treated with vaccinia virus, has been clinically and experimentally reported to demonstrate analgesic effects. In this study, we investigated the antinociceptive action of neurotropin in relation to the serotonergic system, a pain inhibitory system, and substance P, a pain transmitter; we also attempted to determine whether it acts at the spinal or supraspinal level in mice. 1) The spinal cord (T6-T10) transection completely abolished the antinociceptive action of neurotropin, attenuated that of morphine, and had no influence on the action of clonidine. 2) The intrathecal substance P-induced behavior was inhibited by [D-Pro2, D-Trp7, 9]-substance P, but not by neurotropin. 3) Preadministration of p-chlorophenylalanine or cyproheptadine inhibited the antinociceptive action of neurotropin. These data suggest that neurotropin does not directly act on pain transmitters at the spinal cord level, but acts at the supraspinal level, resulting in an inhibition of pain transmitter release at the spinal level by mediating pain inhibitory systems such as the serotonergic system in addition to the noradrenergic and GABAergic systems previously reported.View full abstractDownload PDF (343K) -
Masao KOIDA, Hiromichi NAKAMUTA, Kayoko YASUDA, Keiko MUGURUMA, Yasuzo ...1989 Volume 51 Issue 2 Pages 273-278
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSAn injection of 12.5 ml of carbon monoxide (CO) gas into an air-filled chamber (780 ml in volume) caused the death of the ICR or ddY mouse (6-8 weeks old) inside. The average survival time was 2.5 min for either sex of animals treated with nothing or saline and never exceeded 8 min. Pretreatment with pentobarbital Na (30 mg/kg, i.p.), hopantenate Ca (100 mg/kg, i.p.), vinpocetine (5 mg/kg, i.p. or 50 mg/kg, p.o.), flunarizine HCl (5 mg/kg, i.p.), glucose (6 g/kg, i.p.), phenobarbital (30 mg/kg, i.p.), phenytoin (20 mg/kg, i.p.), arginine HCl (100 mg/kg, i.p. or 1 g/kg, p.o.) and alanine (100 mg/kg, i.p. or 1 g/kg, p.o.) prolonged the survival time of male mice. Insofar as tested, female mice responded rather poorly to these pretreatments. Survival for longer than 8 min occurred in some of the drug-pretreated animals of either sex. To be noted is the finding that most of the animals which survived 8 min once were able to survive the second 8 min on the following day without any drug-treatment. Monitoring of the time course of carboxyhemoglobin formation revealed that the carboxyhemoglobin level reached a plateau of 70% saturation within 2 min and then gradually increased. The lethal level was about 72%. Pentobarbital decreased the formation rate but did not elevate the lethal level. The results indicate that the CO-induced hypoxia model of mice is usable for screening of drug candidates which may be effective for treatment of human ischemic diseases.View full abstractDownload PDF (320K) -
Tamiko SUZUKI-NISHIMURA, Hidehito SEKINO, Yasushi YOSHINO, Kohi NAGAYA ...1989 Volume 51 Issue 2 Pages 279-290
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe effects of synthetic polycations, which induce liposomal membrane fusion without inducing permeability changes, on histamine release from rat mast cells were investigated. Polyethylenimines and polyallylamines with various molecular weights released histamine from mast cells. Acetylated derivatives and triethylentetramine did not release histamine or serotonin from the cells. The histamine release induced by 10 μg/ml polyethylenimine with a molecular weight of 600 was inhibited by 1 mM dibutyryl cyclic AMP, but not by 1 mM 8-bromo cyclic GMP; 100 μM D-600, a calcium antagonist; or 30 μM W-7, a calmodulin inhibitor. In the presence of polyethylenimines with molecular weights of 600, 1, 200 and 1, 800, no detectable release of cytosolic lactate dehydrogenase was observed, indicating that histamine release induced by these polycations was not due to their cytotoxicity. The potencies of these polymers in inducing histamine release depended on their charges, but not on their degrees of polymerization. On the other hand, the actions of polyethylenimine with a molecular weight of 10, 000 and polyallylamines with molecular weights of 3, 000-4, 000 and 10, 000 in releasing lactate dehydrogenase were somewhat cytotoxic. These polycations did not induce serotonin release from rat platelets, suggesting that platelets have no coupling system of signal transduction by these polycations. Thus polycations seemed to interact with the mast cell membrane to induce histamine release, and the potencies of these polycations on mast cells seemed to differ from those of their effects on liposomes, which were examined previously.View full abstractDownload PDF (645K) -
Hironori TANAKA, Koji TAKEUCHI, Susumu OKABE1989 Volume 51 Issue 2 Pages 291-297
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSA single s.c. administration of histamine dose-dependently (5-20 mg/kg) induced villous damage of the proximal duodenum in 24-hr fasting rats. Time course studies indicate that histamine (20 mg/kg) induced severe exfoliation of the epithelial cells at the villous tips of the duodenal mucosa 0.5 hr after administration. The damage, however, tended to heal with time, and recovery was nearly complete 8 hr later. This villous damage was significantly inhibited by pretreatment with sodium bicarbonate given orally or cimetidine, omeprazole and NC-1300 given subcutaneously. Histamine (20 mg/kg) significantly stimulated gastric acid secretion and lowered the intraduodenal pH for 1 hr. Gastric content was significantly greater than that in the control group for 1 hr after histamine administration, probably due to stimulated gastric secretion and delayed emptying. We conclude that a single administration of histamine induces microscopical duodenal damage by stimulation of gastric acid secretion, but the damage heals with time, probably as a result of the short periods of acid stimulation and delayed emptying.View full abstractDownload PDF (475K) -
Akinobu NAGAOKA, Masaki SHIBOTA1989 Volume 51 Issue 2 Pages 299-301
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of manidipine, a new dihydropyridine derivative, on sodium and water excretion were examined in conscious spontaneously hypertensive rats. Manidipine (3 mg/kg) significantly increased the sodium and water excretion in the urine collected for 3 hr after the calcium antagonist was orally administered, and its natriuretic action was more prominent than those of nifedipine and nicardipine (3 mg/kg). These results suggest that manidipine may be useful for treating hypertension.View full abstractDownload PDF (154K) -
Misako KUWAHARA, Takao KUBO, Yoshimi MISU1989 Volume 51 Issue 2 Pages 302-305
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSWe have attempted to clarify whether or not captopril and 1Sar-8lle-angiotensin II could protect isoproterenol-induced facilitation of norepinephrine release in guinea pig pulmonary arteries loaded with 3H-norepinephrine. Angiotensin I at 1 nM and 30 nM isoproterenol similarly facilitated evoked release of 3H-norepinephrine at 1 Hz. Captopril at 1 μM and 1Sar-8lle-angiotensin II at 10 nM completely prevented angiotensin I-induced facilitation, whereas these pretreatments produced no effect on isoproterenol-induced facilitation. Isoproterenol-induced facilitation of norepinephrine release does not primarily involve a local angiotensin II mechanism.View full abstractDownload PDF (207K) -
Nobuyuki OGAWA, Hiroshi ONO1989 Volume 51 Issue 2 Pages 306-308
Published: 1989
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSIn aequorin-loaded human platelets, Bay k 8644 (1-100 μM) had no effect on the resting level of cytoplasmic Ca2+ and did not induce aggregation by itself. Though the rise of cytoplasmic Ca2+ and platelet aggregation induced by thrombin (0.1 U/ml) also was not inhibited by 1-10 μM of Bay k 8644, at concentration of 3-10 μM, it dose-dependently reduced those induced by collagen (5 μg/ml). The present study shows that human platelets do not have dihydropyridine sensitive Ca channels.View full abstractDownload PDF (151K)
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