[Captopril test].
Explore the source record for details and available documents.
Adrenal Cortex Function Tests↗
Biomedical subjects
M Arita
Publications and source records attributed to M Arita.
[Clinical studies with angiotensin II and angiotensin III].
Explore the source record for details and available documents.
Adrenal Cortex↗
Case report of a patient with bilateral renal cell carcinoma successfully maintained on continuous ambulatory peritoneal dialysis after bilateral nephrectomy.
We report on a patient who developed bilateral renal cell carcinoma during continuous ambulatory peritoneal dialysis for chronic renal failure. He was successfully maintained on this type of dialysis after bilateral abdominal nephrectomy.
Adult↗
Sulfatide is expressed in both erythrocytes and platelets of bovine origin.
A novel sulfated glycosphingolipid containing a sulfated galactosyl residue was isolated from bovine erythrocyte ghosts, and purified to homogeneity by column chromatography on DEAE-Sephadex and silica beads. Structural characterization included compositional analyses, permethylation studies, proton nuclear magnetic resonance (NMR) spectroscopy, negative secondary ion mass spectrometry (SIMS), solvolysis and immunostaining on thin-layer chromatogram. As a result, the structure of this glycolipid is proposed as HSO3-Gal beta 1-1 Cer. The ceramide portion contained d18:1, d18:0 and t18:0, and the predominant fatty acid consisted of palmitate and palmitate with a hydroxy group, as deduced by both compositional analysis and negative SIMS mass spectrometry. The component of this glycosphingolipid probably originates from erythrocytes and platelets as indicated by the results of flow cytometry analysis using Sulph I monoclonal antibody. The yield of galactosyl sulfatide was about 0.37 mg/kg wet bovine erythrocyte membranes, about three times that of human kidney. Our results strongly suggest that galactosylceramide sulfate on erythroid cells may play an important biological role in cell to cell interaction and recognition.
Animals↗
Potent immunosuppressants, 2-alkyl-2-aminopropane-1,3-diols.
Several immunosuppressants, ISP-I [(2S,3R,4R)-(E)-2-amino-3,4-dihydroxy-2-(hydroxymethyl)-14-oxoeicos++ +-6-enoic acid, myriocin = thermozymocidin] and mycestericins A-G, were isolated from culture broths of Isaria sinclairii and Mycelia sterilia, respectively. In order to investigate structure-activity relationships, extensive modifications of ISP-I were conducted, and it was established that the fundamental structure possessing the immunosuppressive activity is a symmetrical 2-alkyl-2-aminopropane-1,3-diol. The tetradecyl, pentadecyl, and hexadecyl derivatives prolonged rat skin allograft survival in the combination of LEW donor and F344 recipient and were more effective than cyclosporin A. Among them, 2-amino-2-tetradecylpropane-1,3-diol hydrochloride, ISP-I-55, showed the lowest toxicity. ISP-I-55 is a promising lead compound for the development of effective immunosuppressants for organ transplantations and for the treatment of autoimmune diseases.
Acyltransferases↗
Induction of polymorphic ventricular tachycardia by programmed ventricular stimulation in vasospastic angina pectoris.
This study was designed to examine the ventricular vulnerability of patients with vasospastic angina. Fourteen patients (mean age 57 +/- 9 years) with vasospastic angina underwent electrophysiologic testing during the asymptomatic phase (baseline) and after the relief of acetylcholine-induced spasm with isosorbide dinitrates. Twenty patients without structural heart disease served as a control group. By programmed ventricular stimulation, polymorphic ventricular tachycardia (VT) was induced at baseline in 6 of 14 patients, with 1 patient developing ventricular fibrillation and 7 of 14 patients developing repetitive ventricular responses. After isosorbide dinitrate, polymorphic VT was induced in only 1 patient who had ventricular fibrillation at baseline. Repetitive ventricular responses were induced in 3 of 5 patients who had VT at baseline and in 4 of the 7 patients with repetitive ventricular responses at baseline. There was a significant difference in the incidences and severity of induced ventricular arrhythmias between the 2 phases (p <0.01). Among 20 control subjects, repetitive ventricular responses were induced only in 6 patients, but no VT was induced. There was a significant difference in the incidence of induced ventricular arrhythmias and VT at baseline between the vasospastic angina and control groups (p <0.001 and <0.01, respectively). Thus, patients with vasospastic angina had increased ventricular vulnerability, even during the symptom-free period without ischemic events, which could predispose to the development of life-threatening arrhythmias aggravated by vasospastic attacks.
Adult↗
Comparison of the effects of class I anti-arrhythmic drugs, cibenzoline, mexiletine and flecainide, on the delayed rectifier K+ current of guinea-pig ventricular myocytes.
The effect of class I anti-arrhythmic drugs, cibenzoline, mexiletine and flecainide, on the delayed rectifier potassium current (IK) in guinea-pig ventricular myocytes was studied using whole cell voltage clamp techniques and under blockade of the L-type calcium current by 5 microM nitrendipine. IK consisted of two different current systems, as reported by Sanguinetti and Jurkiewicz (1990), i.e. an E4031-sensitive rapidly activating component (IKr) with a strong inward-going rectification property and an E4031-insensitive slowly activating component (IKs) with little rectification. Cibenzoline (30 microM) decreased both IKr and IKs while flecainide (10 and 30 microM) decreased the IKr exclusively. Mexiletine (30 microM), in contrast, affected neither IKr nor IKs. Since the inhibition of IK(r) and/or IKs prolongs duration of action potentials and refractory periods, class I drugs which also possess the class III effect may have additional effects in treating certain re-entrant arrhythmias.
Action Potentials↗
Hydrocarbon chain length-dependent antagonism of acylcarnitines to the depressant effect of lysophosphatidylcholine on cardiac sodium current.
Amphiphilic lipid metabolites, including lysophosphatidylcholine (lysoPC) and long-chain acylcarnitine, accumulate in an ischemic myocardium and exert deleterious effects on membrane function. The effects of short-chain (3-carbon-chain, C3), medium-chain (C6 and C8), long-chain (C16) acylcarnitines, and lysoPC on the sodium current (INa) of isolated guinea-pig ventricular cells and on membrane fluidity and [14C]lysoPC uptake in cultured mouse embryo ventricular cells were examined. Guinea-pig ventricular cells were superfused with low-Na+(60 mM) Tyrode solution at a temperature of 32-33 degrees C. Ca2+ and K+ currents were blocked by external Co2+(3 mM) and internal Cs+(140 mM), respectively. Neither propionylcarnitine (PpC, C1) nor hexanoylcarnitine (HxoC. C6) at concentrations of 50, 100, 500 microM affected the amplitude of peak LNa, evoked by depolarizing pulses (0.5 Hz) to -20 mV from a holding potential of -100 mV. Octanoylcarnitine (OcoC, C8) (50 and 100 microM) did not alter the amplitude of peak INa while the highest concentration (500 microM) did inhibit it by 7.7 +/- 3.0% (mean +/- S.E., n = 6) significantly. Palmitoylcarnitine (PamC, C16) (1, 5, and 50 microM), decreased the amplitude of peak INa by 16.6 +/- 5.2% (n = 5), 36.1 +/- 4.3% (n = 11), and 52.7 +/- 8.8% (n = 4), respectively. LysoPC (50 microM) irreversibly depressed INa within 30 +/- 4 seconds (n = 4), and cell contracture occurred. If short- and medium-chain acylcarnitines would prevent the depressant effects of lysoPC on INa was then investigated. In the presence of PpC (100 microM) or HxoC (100 microM), the effects of lysoPC (either depression of INa or development of cell contracture) were not observed, while OcoC (100 microM) did not prevent any of these effects of lysoPC. In contrast, PpC and HxoC failed to prevent the reduction of INa caused by PamC. From these findings and membrane fluidity and [14C]lysoPC uptake studies, it was concluded that PpC exerts the protective effect by preventing the incorporation of lysoPC into phospholipid bilayers, and that short-chain acylcarnitine has a potent anti-amphiphilic effect against the amphipathic insults caused by lysoPC, whereas long-chain acylcarnitine had a potent amphiphilic effect; medium-chain acylcarnitine appeared to share both characteristics.
Animals↗
Control of gastric pH with ranitidine in patients with Crohn's disease receiving total parenteral nutrition. Comparison of two intravenous regimens.
Eleven patients with Crohn's disease in remission who were receiving total parenteral nutrition (TPN) underwent continuous intragastric 24-h pH monitoring before and during ranitidine administration. The patients were randomly allocated to receive 200 mg/day (group 1) or 400 mg/day (group 2) of ranitidine by continuous infusion. The mean basal 24-h gastric pH was sustained at a low value. After raintidine administration, the mean pH increased significantly both in group 1 (from 2.13 to 3.28) and in group 2 (from 1.91 to 3.36), with the mean holding-time at pH-3 also increasing significantly in both groups. There were no differences in the mean pH or holding-time at pH-3 between the two groups during ranitidine administration; however, the plasma ranitidine concentration was significantly higher in group 2. These findings indicate that the continuous infusion of a standard dose of ranitidine exerted a maximal inhibitory effect on the sustained hyperacidity induced by TPN, but that this infusion was unable to maintain the intragastric pH level at above 3.5.
Adolescent↗
Diverse inotropic effects of 5-hydroxytryptamine in heart muscles of various mammalian species.
The inotropic effects of 5-hydroxytryptamine (5-HT) on mammalian heart muscles were investigated. 5-HT (10(-8)-10(-3)M) produced increases in the contractile tension of atrial and ventricular muscles isolated from guinea pigs, Japanese monkeys, and humans, but not in rat heart preparations. The maximum percent increase of contraction was largest in guinea pig ventricular muscles (142.0 percent), followed by monkey atrium (86.3 percent), human atrium (71.7 percent), guinea pig atrium (48.7 percent), and monkey ventricle (30.1 percent). The sensitivity to 5-HT, measured as the negative logarithm of the half-maximal inotropic molar contractions of 5-HT, i.e., -logEC(50), was highest in the human atrium (6.65 +/- 0.20), followed by guinea pig atrium (5.53 +/- 0.36), monkey ventricle (4.83 +/- 0.28), guinea pig ventricle (4.56 +/- 0.11), and monkey atrium (4.46 +/- 0.16). The inotropic effects of 5-HT seen in the atrial and ventricular muscles of guinea pigs were abolished in the presence of the beta-receptor blocker, pindolol (8 mu M), while these effects in human atrial muscles and monkey atrial and ventricular muscles were abolished only in the presence of both pindolol (8 mu M) and of prazosin (1 mu M), an alpha(1)-receptor blocker. 5-HT increased the V(max) of the slow response recorded from guinea pig ventricular muscles exposed to high K+ (27 mM) media, whereas this agent did not alter the calcium current of isolated guinea pig ventricular myocytes devoid of sympathetic nerve terminals. In reserpinized guinea pig hearts, 5-HT exerted no inotropic effect on ventricular muscle, yet it had an inotropic effect in the atrial muscle, although the latter effect was considerably depressed, compared to that seen in non-reserpinized atrial muscles. We conclude that the positive inotropic effects of 5-HT observed in the ventricular muscle of the guinea pig and in the atrial and ventricular muscles of the Japanese monkey can be attributed to the release of noradrenaline from sympathetic nerve terminals (indirect effect). In contrast, in human atrial muscles, the positive inotropic effect of 5-HT was apparently the result of stimulation of a specific membrane receptor for 5-HT (direct effect). In guinea pig atrial muscles, both direct and indirect effects of 5-HT were involved in the positive inotropism. An explanation for the lack of sensitivity of rat atrial and ventricular muscles to 5-HT awaits further studies.
Adrenergic Fibers↗
Measurement of intact rat osteocalcin in osteoblast (ROS17/2.8) cells and in ovariectomized rats with a sandwich enzyme immunoassay.
We developed a sandwich enzyme immunoassay system for intact rat osteocalcin to improve the region specificity for the detection of this molecule. We synthesized two peptides of N-terminal 20 residues and C-terminal 10 residues of rat osteocalcin. After conjugating these peptides with carrier protein, we obtained anti-N- and anti-C-terminal rat osteocalcin antibodies in rabbits raised against these two peptides, respectively. By using these antibodies, we measured intact rat osteocalcin levels in a two-site immunoassay manner. These antibodies did not show the cross-reactivity to human osteocalcin. The immunoreactive peak corresponding to the intact molecules was detected by our intact osteocalcin method after high-performance liquid chromatographic fractionation of osteocalcin fragments in plasma from uremic rats. Furthermore, the intact rat osteocalcin was stable over 8 hours at 25 degrees C. Intact rat osteocalcin levels extracellularly secreted from ROS 17/2.8 cells were measured by this method, showing time- and dose-dependent significant increases when administered 1,25(OH)2D3. The inhibition for the secretion of intact osteocalcin by actinomycin D was also detected quantitatively with this method. In ovariectomized rats, intact osteocalcin levels in plasma were acutely elevated after ovariectomy, and its elevation was significantly depressed by 17beta-estradiol administration. These data suggest that this sandwich method is able to measure the intact form of osteocalcin secreted by osteoblasts. As the antibodies identify the specific regions of osteocalcin molecule, this method would be useful for sensitive estimation of bone turnover for various experimental conditions in rats.
Animals↗
Impaired glucose tolerance with late hypersecretion of insulin during oral glucose tolerance test in patients with vasospastic angina.
OBJECTIVES: This study tested whether patients with vasospastic angina have impaired glucose tolerance or impaired insulin response. BACKGROUND: Hyperinsulinemia has been demonstrated in patients with coronary artery disease and syndrome X. METHODS: We performed an oral glucose tolerance test (75 g) in 30 patients with vasospastic angina in whom severe coronary vasospasm was induced by acetylcholine and in a matched group of 30 patients with atypical chest pain in whom no significant vasospasm was induced. The responses of insulin and glucose were compared between the two groups. No subjects had overt diabetes mellitus, hypertension, dyslipidemia, obesity or angiographically detected significant baseline coronary stenosis. Venous blood samples were taken during fasting and at 30, 60, 120 and 180 min after glucose load to obtain plasma glucose and immunoreactive insulin levels. RESULTS: Impaired glucose tolerance was detected in the 19 (63%) of 30 patients with vasospastic angina and in none of 30 patients with atypical chest pain (p < 0.001). The immunoreactive insulin levels at 60 and 120 min as well as the interval to peak insulin level were significantly greater in patients with vasospastic angina (p < 0.001). Among patients with vasospastic angina, those with acetylcholine-induced multivessel coronary vasospasm showed a significantly higher sum of insulin concentrations than those with single-vessel spasm (p < 0.01). During induction of coronary spasm, 10 patients with vasospastic angina presented ventricular arrhythmias. The sum of insulin concentrations was significantly greater in patients with than in those without ventricular arrhythmias. CONCLUSIONS: Patients with vasospastic angina exhibited a high incidence of impaired glucose tolerance and delayed and significantly higher insulin responses. These findings suggest that impaired glucose tolerance with late hypersecretion of insulin may contribute to the pathogenesis of severe coronary vasospasm.
Adult↗
Pathogenic role of thromboxane A2 in immediate food hypersensitivity reactions in children.
BACKGROUND: Food hypersensitivity, from the standpoint of pathogenesis as well as clinical management, remains controversial. During the food allergen-induced immediate hypersensitivity reaction, various chemical mediators are released. OBJECTIVE: The purpose of our study was to determine whether thromboxane A2 participates in food antigen-induced responses in children with food hypersensitivity. METHODS: Nine open food challenges were performed in nine patients with suspected food hypersensitivity. Plasma thromboxane B2 and histamine levels were measured during a 24-hour period following the challenge. RESULTS: All the patients demonstrated immediate reactions after food challenge. The mean plasma thromboxane B2 level (a marker of thromboxane A2 activity) rose significantly at two hours and three hours after the challenge. Simultaneously, the mean plasma histamine level rose significantly at two hours and three hours after the challenge. CONCLUSIONS: The results suggest that thromboxane A2 may play a pathogenic role in part in the immediate reaction after food challenge and that thromboxane A2 is probably released from a common cellular source (eg, mast cell) with histamine and/or by a common mechanism (eg, IgE-dependent platelet activation).
Child↗
Unique genomic structure and expression of the mouse alpha 2,8-sialyltransferase (ST8Sia III) gene.
The mouse Sia alpha 2,3Gal beta 1, 4GalNAc alpha 2,8-sialyltransferase (ST8Sia III) genomic gene, whose transcripts are only expressed in fetal and newborn brain and testis, was isolated and its 5'-flanking region was analyzed. The gene was found to span about 8 kb and to be composed of only four exons. The genomic ST8Sia III gene is much smaller and its organization much simpler than other sialyltransferase genes so far reported, which span more than 25 kb and comprise seven or more exons. In particular, the sialyl motif L of ST8Sia III, which is a highly conserved region in all cloned sialyltransferases, was in one exon. In contrast, this motif is encoded by discrete exons in the other sialyltransferases. The ST8Sia III gene was highly expressed in the mouse brain and gave rise to at least three transcripts (2.1 kb, 2.4 kb, and 6.5 kb), which differed in the length of their 3'-untranslated regions through the alternative use of different polyadenylation sites. Primer extension and S1 nuclease protection analyses of mRNA prepared from newborn brain revealed that ST8Sia III gene expression started from a unique site at 382 nt upstream of ATG. Although the promoter region lacked an apparent TATA or CCAAT box and potential regulatory motifs, a transfection experiment involving neuroblastoma cells expressing ST8Sia III demonstrated the minimal promoter activity exhibited by the proximal region 418 bp upstream from the ATG codon, which suggests the presence of tissue-specific enhancer elements.
3T3 Cells↗
Openings of cardiac KATP channel by oxygen free radicals produced by xanthine oxidase reaction.
We examined the effects of oxygen free radicals (OFRs) on action potentials and membrane currents of guinea pig ventricular myocytes. OFRs produced biphasic changes in the action potential duration, initial lengthening (30 s after exposure to OFRs) and subsequent shortening (within 5 min). In voltage-clamp experiments, OFRs suppressed the L-type calcium current, the delayed rectifier K+ current, and the inward rectifier K+ current. In addition, OFRs increased the time-independent outward current (I(term)) at potentials greater than -30 mV. The increases in I(term) reflected activation of the ATP-sensitive K+ (KATP) channels, as glibenclamide (1 microM) blocked this current. In inside-out patches, OFRs significantly increased the open probability of the channel at a relatively narrow range of ATP concentrations (0.2-2 mM), and this effect was enhanced in the presence of ADP (0.1 mM) and abolished in the presence of either free radical scavengers or gliben-clamide. These findings are compatible with the notion that OFRs activate KATP channels by modulating ATP binding sites of the KATP channels, without affecting ADP binding or glibenclamide binding sites.
Action Potentials↗
GM1b is a new member of antigen for serum antibody in Guillain-Barré syndrome.
Serum antibody from some patients with Guillain-Barré syndrome recognized an antigen of a minor component in human brain monosialoganglioside fraction. We purified that antigen, which migrated at a position slightly lower than that of GM1 on a thin-layer chromatogram (TLC), by using Iatrobeads column chromatography and preparative TLC. Structural analyses, including fast atom bombardment mass spectrometry, showed it to be GM1b. An enzyme-linked immunosorbent assay (ELISA) using purified GM1b showed that anti-GM1b antibody was present in 22 of 104 cases tested. No anti-GM1b antibody was present in the sera from control patients with other diseases or from the normal controls. Four sera recognized only GM1b among the 11 ganglioside antigens tested. The other 18 sera had antibodies to other antigens, most of which shared no terminal epitope with GM1b. Eight of nine sera samples with anti-GalNAc-GD1a antibody also had anti-GM1b antibody. Antibody to a minor monosialoganglioside, GM1b, was found to be a useful diagnostic marker for Guillain-Barré syndrome. Further study is needed to determine whether this antibody plays a role in the pathogenetic mechanism of the syndrome.
Carbohydrate Sequence↗
Purification and characterization of N-acetylglucosamine 6-phosphate deacetylase with activity against N-acetylglucosamine from Vibrio cholerae non-O1.
An enzyme that deacetylates N-acetylglucosamine to glucosamine from Vibrio cholerae non-O1 was purified to homogeneity by sequential procedures. The native enzyme had a molecular mass of 190,000 Da and was predicted to be composed of four identical subunits with molecular masses of 45,000 Da. The purified enzyme hydrolyzed N-acetylglucosamine, N-acetylglucosamine 6-phosphate, and N-acetylglucosamine 6-sulfate, but not chitin oligosaccharides, and N-acetylgalactosamine. The deacetylase activity was completely abolished by N-ethylmaleimide, p-chloromercuribenzoate, EDTA, and Cu2+. On the other hand, the activity was activated by Co2+. The amino-terminal amino acids of the purified enzyme were sequenced. Among the 22 N-terminal amino acid residues, 12 residues of Vibrio deacetylase were identical with that of Escherichia coli GlcNAc 6-phosphate deacetylase.
Acetylglucosamine↗
Role of the sympathetic nervous system in the nocturnal fall in blood pressure.
To evaluate mechanisms responsible for differences between patients showing a nocturnal fall in blood pressure ("dippers") and those showing no such fall in blood pressure ("nondippers"), we performed 24-hour (h) ambulatory blood pressure monitoring in 25 patients with untreated essential hypertension who were 37-49 years of age (16 men and 9 women). The diagnosis of essential hypertension was based on the patients' history, physical examination, routine laboratory tests, and intravenous pyelography. Blood pressure was measured by sphygmomanometer and by noninvasive ambulatory monitoring for 24 h. Exercise was performed on a supine bicycle ergometer. The initial workload was 50 W and was increased progressively by 25 W at 3-min intervals. Plasma and urinary norepinephrine levels were measured by high-performance liquid chromatography. Dippers were defined as patients with a difference of > 10 mmHg in the systolic BP or > 5 mmHg in the diastolic BP between daytime and nighttime. Eleven patients were dippers and 14 patients were nondippers. There was a positive correlation between the nocturnal fall in blood pressure and the rise in blood pressure during exercise (r = 0.54, p < 0.01), and the increase during exercise was greater in dippers than in nondippers. There was also a significant positive correlation between the urinary norepinephrine level and the fall in blood pressure at night (r = 0.75, p < 0.01). A significant increase in plasma norepinephrine during exercise was found in dippers, as compared with nondippers. These results suggest that in patients with hypertension a nocturnal fall in blood pressure is closely related to the blood-pressure response to exercise, and that the attenuation of sympathetic nervous activity might play an important role in the nocturnal decrease in blood pressure.
Adult↗