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Volume 29 (1979)
- Issue 6 Pages 821-
- Issue 5 Pages 687-
- Issue 4 Pages 503-
- Issue 3 Pages 319-
- Issue 2 Pages 151-
- Issue 1 Pages 1-
Volume 29, Issue 2
Displaying 1-21 of 21 articles from this issue
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Mehdi SALIMI, Mohammad A. KHOYI, Monir A. DIBAI1979 Volume 29 Issue 2 Pages 151-160
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe effect of ethacrynic acid on the motor function of guinea pig ileum was studied in vitro. Ethacrynic acid produced dose-related (5-160 μg/ml) contractions in this tissue. Morphine, tetrodotoxin and sodium-free medium prevented the contractions while hexamethonium, diphenhydramine, methysergide or indomethacin did not. Atropine in a high concentration (0.1 μg/ml) only inhibited the contractions. Ethacrynic acid inhibited the contraction of ileum induced by electrical stimulation of intramural nerves. This was not prevented by pretreatment with reserpine. Repeated exposure to ethacrynic acid developed tachyphylaxis in contractile response. Inhibition of electrically elicited contraction of guinea pig ileum also diminished with repeated treatment. Ethacrynic acid (80-160 μg/ml) inhibited the peristaltic reflex of the guinea pig ileum. It is concluded that the excitatory effect of ethacrynic acid is most probably mediated by the release of neurotransmitter, however, the mechanism of the inhibitory effect remains to be elucidated.View full abstractDownload PDF (572K) -
Kyoichi SHIMOMURA, Masaharu HASHIMOTO, Jo MORI, Fumio HONDA1979 Volume 29 Issue 2 Pages 161-170
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSTranylcypromine (TCP), a monoamine oxidase inhibitor, caused a fatal hyperpyrexia in rats pretreated with LiCl once a day for 4 days. Pretreatment with LiCl alone did not alter the level of serotonin (5-HT). dopamine (DA) and norepinephrine (NE) in the brain. In the fatal hyperpyrexia caused by LiCl plus TCP, the brain 5-HT and DA levels were increased, whereas the brain NE level was decreased. Reserpine and α-methyl-p-tyrosine completely prevented the hyperpyrexia, but FLA-63 did not show any effect. The hyperpyrexia was completely prevented by p-chlorophenylalanine (PCPA) given 72 hours before TCP but not by PCPA given 24 hours before TCP. Haloperidol and chlorpromazine, DA receptor blockers, inhibited the fatal hyperpyrexia, while cyproheptadine and inethysergide, 5-HT receptor blockers, did not. These results suggest that DA plays an essential role in the hyperpyrexia induced by the combination of TCP and LiCl in rats, but the involvement of 5-HT is inconclusive.View full abstractDownload PDF (620K) -
Keisuke TAKEDA, Yoshito NAKAGAWA, Toyozo HASHIMOTO, Hiroshi SAKURAI, S ...1979 Volume 29 Issue 2 Pages 171-178
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSAntihypertensive effects of chronic oral administration of adrenergic β-blocking agents were assessed in SHR. Propranolol, pindolol, oxprenolol, atenolol and labetalol were used as β-blockers and the effects of these compounds on the blood pressure and the heart rate were compared with those of hydralazine, a representative vasodilating antihypertensive agent. Propranolol, oxprenolol and atenolol produced a definite decrease in the heart rate, the development of hypertension was retarded. Pindolol produced antihypertensive effects only after a longer period of administration and such were associated with insignificant decrease in heart rate. With a shorter period of administration the drug produced only an insignificant fall of blood pressure with practically no change in the heart rate. With labetalol, a β-blocker with α-blocking action, a fall of blood pressure appeared earlier and was of greater magnitude. Hydralazine produced a definite antihypertensive effect, which appeared immediately after administration and was associated with a tachycardia. In pithed rats, only pindolol produced a definite fall of blood pressure. On the basis of these findings, possible mechanisms of antihypertensive effects of β-blockers were discussed.View full abstractDownload PDF (505K) -
Yasusuke MASUDA, Tadashi MURANO1979 Volume 29 Issue 2 Pages 179-186
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSRat liver microsomes incubated with linoleic acid hydroperoxide (LAHPO) lost cytochrome P-450 specifically among the enzymes of microsomal electron transport systems. The loss of cytochrome P-450 content and glucose-6-phosphatase activity by LAHPO was accompanied by an increase in malondialdehyde (MDA) production. Turbidity of microsomal suspensions was decreased with increasing MDA production, but not proportionately. Diethyldithiocarbamate (DTC), N, N'-diphenyl-p-phenylenediamine and α-tocopherol inhibited almost completely the LAHPO-induced MDA production of microsomes, however no perfect protection against the loss of cytochrome P-450 content and glucose-6-phosphatase activity was observed. The decrease of microsomal turbidity by LAHPO was little affected in the presence of DTC. Purified cytochrome P-450 was destroyed by LAHPO, with minimal protection by the compounds described above. These results suggest the possibility that the loss of microsomal enzyme activities during lipid peroxidation may be attributed largely to a direct attack on enzyme proteins by lipid peroxides rather than indirectly to a structural damage of microsomal membranes resulting from peroxidative breakdown of membrane lipids.View full abstractDownload PDF (517K) -
Kazuhiko IWATSUKI, Koroku HASHIMOTO1979 Volume 29 Issue 2 Pages 187-190
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSEffect of 5-dimethyldithiocarbamylpicolinic acid (YP-279), a dopamine β-hydroxylase inhibitor, on the secretion of pancreatic juice induced by dopamine was investigated in preparations of the isolated blood-perfused canine pancreas. Either a single injection (300 μg) or an infusion (100 μg/min) of YP-279 intra-arterially (i.a.) caused no change in the outflow of the pancreatic juice, but the secretagogue effect of dopamine (1-10 μg, i.a.) was enhanced by the infusion of YP-279 (100 μg/min, i.a.) for 60 min. The previous conclusion obtained with fusaric acid was confirmed as follows; the dopamine β-hydroxylase activity controls the dopaminergic mechanism of the pancreatic secretion.View full abstractDownload PDF (224K) -
Tetsuya KAMATAKI, Mitsukazu KITADA, Hidenari SHIGEMATSU, Haruo KITAGAW ...1979 Volume 29 Issue 2 Pages 191-201
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThese studies have shown that addition of p-nitroanisole to a reaction mixture containing rat liver microsomes resulted in an increase the reoxidation rate of NADH-reduced cytochrome b5. Fortification of rat liver microsomes with partially purified cytochrome b5 produces an increase in both NADPH-dependent and NADH-dependent p-nitroanisole O-demethylation activity. Antiserum to cytochrome P-450 isolated from phenobarbital-treated rat liver microsomes inhibited the NADH-dependent O-demethylation activity as well as the NADPH-dependent O-demethylation activity seen in rat liver microsomes. Addition of either purified cytochrome P-450 or cytochrome P-448 to an incubation mixture containing phenobarbital-treated rat liver microsomes enhanced the NADH-dependent p-nitroanisole O-demethylation activity. These results suggest that NADH-dependent and, in part, NADPH-dependent O-demethylations are catalyzed by cytochrome P-448 and cytochrome P-450 receiving electrons from cytochrome b5.View full abstractDownload PDF (745K) -
Masakatsu TAKAHASHI, Hiroshi KANETO, Eiko UENO, Joe WATANABE, Masao KO ...1979 Volume 29 Issue 2 Pages 203-209
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSWe developed a radioimmunoassay of methionine-enkephalin (met-enk) which was found to be highly specific to the peptide and I pmole was the detection limit. Interference by the following peptides was practically negligible; leucine-enkephalin, LAP- or CNBr-treated met-enk, α- and β-endorphins. Morphine and its congeners were totally inert. Measurement of met-enk in rat brain P2 fraction revealed besides met-enk, the presence of the factor which cross-reacted with the antiserum and also appeared to bind with the brain opiate receptor. Though the nature of the factor has not yet been characterized, it is suggested that for qualitative assessment of the tissue level of met-enk, a method to selectively inactivate either the peptide or the factor should be developed first.View full abstractDownload PDF (420K) -
Yukio YONETANI, Mitsuo ISHII, Yasunao OGAWA1979 Volume 29 Issue 2 Pages 211-221
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe effect of catecholamine in vivo was studied on purine catabolism in rats and chickens. Catecholamine, administered intraperitoneally in a high dose, markedly increased plasma uric acid and allantoin in rats, and an increase was also observed with intravenous infusion of a lower dose of catecholamine. The effects of catecholamine were characterized by inhibition with alpha and beta adrenoceptor antagonists. Regarding the mechanism of this catecholamine action on purine catabolism, it was shown that catecholamine stimulated degradation of tissue ATP into the end-product. Plasma allantoin, the final purine catabolite in rats, elicited by catecholamine could be maintained under conditions of renal failure, although the action of catecholamine in intact rat was short lasting. The effect of catecholamine was potentiated and/or prolonged by angiotensin-II and aminophylline, and a hyperuricemic state could be induced by catecholamine treatment in chickens. In addition, increase of plasma purine catabolite by immobilization stress in rats suggested the involvement of endogenous catecholamine. From these experimental results, it is considered that catecholamines probably play a important role in the pathogenesis of hyperuricemia.View full abstractDownload PDF (659K) -
Kazushige SAKAI, Michitaka AKIMA, Yasuyuki SHIRAKI1979 Volume 29 Issue 2 Pages 223-233
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe mode of actions of' 5-hydroxytryptamine (5-HT) and its derivatives, tryptophan (TP), 5-hydroxytryptophan (5-HTP) and 5-hydroxyindole acetic acid (5-HIAA) vas studied on the isolated, blood-perfused small intestine and isolated ileum strip of rats. In the isolated, blood-perfused intestinal preparations, 5-HT and 5-HTP injected into the superior mesenteric artery caused a monophasic fast contraction, while TP and 5-HIAA had no effects on the intestine. The contractile responses to 5-HT and 5-HTP were abolished by tetrodotoxin (TTX), hexamethoitium (C6) and morphine, but were resistant to blockade of either atropine, methysergide or phentolamine. On the other hand, in the ileum strip preparations, 5-HT contracted the ileum, but its derivatives had no effects on the ileum. TTX, C6, morphine and atropine failed to prevent the contractile response to 5-HT, whereas methysergide effectively antagonized the response. The present results indicate that 5-HT acts by exciting intramural neuronal elements or by directly contracting the smooth muscle of the intestine. 5-HTP seems to act in the same manner as 5-HT.View full abstractDownload PDF (630K) -
Kazushige SAKAI, Michitaka AKIMA, Hiroyuki NABATA1979 Volume 29 Issue 2 Pages 235-242
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe isolated kidney of the recipient rat was perfused at a fixed flow rate with blood from a donor by a cross-circulation technique. The renal vasculature responded to the release of arterial occlusion with vasoconstriction, the magnitude of which was increased with increase in the duration of occlusion. ATP, ADP, AMP, adenosine. noradrenaline and 5-HT injected into the renal artery induced a prominent vasoconstriction; IMP and inosine had only a weak vasoconstrictor effect even in large doses. Theophylline reduced the vasoconstriction in response to arterial occlusion and to ATP and adenosine but did not affect that produced by noradrenaline or 5-HT. This suggests that adenine compounds, particularly adenosine, may play a role in the genesis of reactive vasoconstriction after arterial occlusion in the isolated rat kidney.View full abstractDownload PDF (482K) -
Kazushige SAKAI, Michitaka AKIMA, Hiroshi MATSUSHITA1979 Volume 29 Issue 2 Pages 243-251
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe mode of actions of the purines, adenosine, adenosine-5'-triphosphate (ATP), guanosine and guanosine-5'-triphosphate (GTP), and the pyrimidines, cytidine, cytidine-5'-triphosphate (CTP), thymidine, thymidine-5'-triphosphate (TTP), uridine and uridine-5'-triphosphate (UTP) was investigated in the isolated hindlimb preparation of the rat. A single injection of adenosine, ATP, GTP or UTP into the femoral artery induced a biphasic response, a prominent vasoconstriction preceded by a transient vasodilatation, whereas guanosine and uridine caused only a vasoconstriction. Cytidine, CTP, thymidine and TTP were almost ineffective on the vascular bed. The vasoconstrictor responses to adenosine, ATP, guanosine and GTP were effectively antagonized by either methysergide or reserpine, whereas those to uridine and UTP were not modified by either methysergide or phentolamine. Adenine, D-(-)-ribose and hypoxanthine had no effect on the vascular bed. The 5-hydroxytryptamine (5-HT) release from the hindlimb was fluorometrically determined. The present results provide direct evidence that the vasoconstriction caused by ATP, adenosine, GTP and guanosine is attributed to the release of 5-HT from their stores and that purine nucleotides and nucleosides are capable of releasing 5-HT.View full abstractDownload PDF (509K) -
Masayasu KIMURA, Ikuko KIMURA1979 Volume 29 Issue 2 Pages 253-260
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSExtracts of 5% glycerol obtained from ox diaphragm muscles were fractionated into four (A, B, C and D) with (NH4)2SO4. The activity as acetylcholine (ACh) receptor-like substance containing fraction was evidenced as follows; the ACh-induced contraction of tracheal muscles decreased with addition of the fraction, and such could not be attributed to the reaction with ACh receptors of tracheal smooth muscles. Fraction D had the most potent activity in the presence of neostigmine. This reaction induced by fraction D was reversed by addition of d-tubocurarine(d-TC). Fraction D was fractionated into three (I, II and III) by gel filtration on Sephadex G-75 with 50 mM phosphate buffer (pH 7.5). The purified fraction III was identified by electrophoresis, UV and visible absorption spectrum, and ion-exchange chromatography to be myoglobin. Pure myoglobin also proved to have a decreasing effect on ACh-induced contraction.View full abstractDownload PDF (512K) -
Masao SATO, Tatsuya TAKANO1979 Volume 29 Issue 2 Pages 261-269
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSRegression mechanism of Ethyl 2-(p-chlorophenoxy) isobutyrate (CPIB) in the arterial wall was studied for elucidation in terms of fatty acid-compositional change in cholesterol-fed rabbits. The following evidence was obtained: (1) The amount of cholesterol and cholesteryl ester in the atheromatous aorta were reduced after CPIB treatment. (2) CPIB resulted in a significant increase in the ratio of linoleate to oleate in both the arterial wall and serum after withdrawal of the cholesterol diet. It is suggested that there is a preferential hydrolysis of linoleate-rich cholesteryl ester in both the arterial wall and the serum.View full abstractDownload PDF (575K) -
Yoshito NAKAGAWA, Keisuke TAKEDA, Yumi KATANO, Issei MATSUBARA, Hiroyu ...1979 Volume 29 Issue 2 Pages 271-283
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSTo determine whether or not the development of collateral channels can be accelerated by administration of vasodilators and whether the opening up of functional collateral channels is associated with an improved survival rate, a gradual occlusion of the major branches of the left coronary artery was produced in miniature swine with an Ameroid constrictor. Oral administration of drugs (twice a day) was started seven days before operation and was continued throughout the experimental period of 2 months. While the survival rate of the untreated animals was 6/15 (40%), survival rates of animals treated with adenosine potentiators, dipyridamole and dilazep were 4/7 (57.1%) and 5/7 (71.4%), respectively. However, a significant improvement of the survival rate was attained by KI 2119, survival rate was 6/7 (85.7%). Coronary angiography of the survived control animals revealed numerous, fine, collateral communications between the left and right coronary arteries. Treatment with dipyridamole and dilazep resulted in formation of a dense network of thick collaterals. To quantitate the degree of formation of the collateral channels, the anatomic anastomotic indices (AAI's) were calculated using histological specimens of the anterior free wall of the left ventricle. According to Menick et al. (16), AAI is a good measure of the functional capacity of the collateral vessels. AAI's of the animals treated with dipyridamole and dilazep were 2416.6±454.0 and 1864.7±248.3 as compared with 704.3±407.9 of the untreated animals. AAI's of the KI 2119-treated animals did not differ from those of the control animals. A linear correlation was observed between the survival rate and AAI's (r=0.74, p<0.05), indicating a close relationship between the survival rate and the development of functional collateral channels.View full abstractDownload PDF (1034K) -
Michael J. ANTONACCIO, Bernard RUBIN, Zola P. HOROVITZ, Robert J. LAFF ...1979 Volume 29 Issue 2 Pages 285-294
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe effects of hydralazine (3 mg/kg) and the angiotensin I-converting enzyme (ACE) inhibitor captopril (SQ 14, 225) (100 mg/kg) on mean arterial blood pressure, plasma renin activity, urinary volume and urinary Na+, K+, and aldosterone concentrations were examined in spontaneously hypertensive rats of the Okamoto and Aoki strain (SHR) after oral daily dosing for 2 weeks, 3 or 6 months. Captopril caused progressive cumulative reductions in blood pressure resulting in normalization of pressure after 6 months of dosing. Hydralazine also significantly reduced blood pressure but not to the level of normotensive rats of the Wistar-Kyoto strain (WKY). Reductions in heart size paralleled the changes in blood pressure, normalization of cardiac hypertrophy occurring after captopril but not hydralazine. Plasma renin activity increased approximately 2-3 fold after hydralazine and 15-fold after captopril. Neither hydralazine nor captopril had any consistent effects on 24-hr urine volume, urinary Na+, K+ or aldosterone excretion. These results indicate that chronic inhibition of ACE with captopril induces normalization of blood pressure in SHR, a normal-renin model of hypertension.View full abstractDownload PDF (600K) -
Shizuo YAMADA, Eiichi HAYASHI1979 Volume 29 Issue 2 Pages 295-302
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSEffects of surugatoxin (SGTX), a new ganglionic blocking agent on adrenergically innervated tissues: guinea pig isolated atria and vas deferens were investigated. SGTX (1, 10 μM) markedly reduced the cardiostimulatory response of the atria to nicotine and also partially the response to 1, 1-dimethyl-4-phenylpiperazinium (DMPP) and 5-hydroxvtrvptamine, without affecting responses to noradrenaline, tyramine and histamine. The contractile response of the vas deferens to nicotine, DMPP and hypogastric nerve stimulation was markedly reduced by SGTX (1, 10 μM), whereas that to noradrenaline, acetylcholine and transmural stimulation was not affected. These results indicate that SGTX has an antagonistic action on nicotinic receptors in these tissues as well as in sympathetic ganglia and in guinea pig ileum.View full abstractDownload PDF (444K) -
Makoto SATO, Hisayuki TANIZAWA, Tamotsu FUKUDA, Tomokazu YUIZONO1979 Volume 29 Issue 2 Pages 303-306
Published: 1979
Released on J-STAGE: December 19, 2006
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Yasuyuki NOMURA, Tomio SEGAWA1979 Volume 29 Issue 2 Pages 306-309
Published: 1979
Released on J-STAGE: December 19, 2006
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Kazuo NAKAGAWA, Kinya KURIYAMA1979 Volume 29 Issue 2 Pages 309-313
Published: 1979
Released on J-STAGE: December 19, 2006
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Yutaka KASUYA, Nagao SUZUKI1979 Volume 29 Issue 2 Pages 313-315
Published: 1979
Released on J-STAGE: December 19, 2006
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Heitaroh IWATA, Sadaaki MAEDA, Yoshihisa HIRATA, Toshio MATSUDA1979 Volume 29 Issue 2 Pages 316-318
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSDownload PDF (165K)
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