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Biomedical subjects

Y Takata

Publications and source records attributed to Y Takata.

At least 271 records · Page 15Linked to original sources
PubMed1983

Leakage of angiotensin converting enzyme inhibitors from the cerebral ventricles into the peripheral circulation in conscious, spontaneously hypertensive rats.

The inhibitory effects of SQ14225 and MK421 injected into the lateral brain ventricle (i.c.v.) and intravenously (i.v.) on pressor responses to intravenous (i.v.) angiotensin I(AI, 400 ng/kg i.v.) were compared in conscious spontaneously hypertensive rats (SHR). Both the i.c.v. and i.v. inhibitors suppressed the increase in blood pressure produced by intravenous injections of AI in a dose dependent manner. The inhibition of pressor responses to i.v. AI were rapid in onset and decayed with time following i.v. captopril and MK421, while the effects of i.c.v. inhibitors were slower in onset and were maintained for a longer time. The activity of MK421, either i.v. or i.c.v. persisted for longer compared to that of SQ14225 in conscious SHR. It was concluded that SQ14225 and MK421 readily leaked from the brain ventricles to the peripheral circulation and this observation suggested that the central hypotensive effects of these inhibitors might be partly attributed to peripheral blockade of angiotensin I conversion in conscious SHR.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1983

Effect of DOCA-salt on angiotensin dependency and surgical reversal of hypertension in two-kidney, one clip renal hypertensive rats.

The development of hypertension in two-kidney, one clip renal hypertensive rats (2K, 1C RHR) was not altered by treatment with DOCA and saline solution as drinking fluid for two months of observation. However, the administration of DOCA and salt suppressed plasma renin activity (PRA), the renal renin content (RRC) of the clipped kidney and the response to a single oral dose of captopril (10 mg/kg). The weight of the contralateral kidney was increased by the administration of DOCA-salt, while that of the ischaemic kidney was not changed. The withdrawal of DOCA-salt treatment restored the PRA and the effects of captopril to a similar degree to the non-treated group. The acute hypotensive effects of captopril were reduced on the 10th week compared with the 7th week after renal arterial constriction in 2K, 1C RHR. The fall in blood pressure induced by captopril significantly correlated with the initial PRA both in the 7th and 10th week after clipping. There was a significant correlation between PRA and RRC of the clipped kidney. Rats previously treated with DOC-salt had either removal of the contralateral kidney with removal of the clip from the ischaemic kidney, or removal of the ischaemic kidney. Blood pressure fell to normal levels in the unclipped group and in the nephrectomy group, but the fall in the latter group was transient and within two weeks had risen to significantly higher levels than in the unclipped group. It is concluded that structural vascular change following DOC-salt hypertension is insufficient to cause persisting hypertension except when it occurs in the renal circulation.

Animals↗
PubMed1982

Computed tomography of malignant tumors of the nasal cavity and paranasal sinuses.

Staging of malignant tumors of the nasal cavity and paranasal sinuses by computed tomography (CT) was studied in a total of 49 patients, 33 with squamous cell carcinoma and 16 with tumors of other histologic types. Involved sites by the tumor were studied, and clinical staging was made using CT findings alone according to AJC classification for maxillary sinus tumors. Surgical findings for comparison were available for most cases. Of 33 squamous cell carcinomas and of 16 tumors with other histologic types, the maxillary sinus was the site of origin in 29 and eight, respectively. Of these 37 maxillary sinus tumors, 11 were staged T3, 26, T4, and none was staged T1 or T2. None of these tumors were down staged, and one T3 was upstaged after surgical procedures, although all sinuses were not explored in some cases. Sinusitis due to obstruction was indistinguishable from the tumor without bone destruction. And the determination of the site of origin was difficult in some cases. Despite these, CT should be used for pretreatment evaluation of the tumors of these sites.

Adenocarcinoma↗
PubMed1982

Analysis of body functions using a clinical liquid chromatograph.

A clinical liquid chromatograph, which consists of a completely automated liquid chromatograph combined with a microcomputer for diagnosis, and its application to body function analyses are described. The analytical rate for urinary ultraviolet-absorbing constituents using anion-exchange chromatography was 12 samples per day, and the reproducibilities for retention time and peak area were less than 3% and 4%, respectively. Diagnostic methods for kidney functions using the chromatograms are discussed.

Adolescent↗
PubMed1982

Dissociation of dipsogenic and pressor responses to chronic central angiotensin II in rats.

Chronic intracerebroventricular (icv) infusion of angiotensin II (ANG II) (6 micrograms/h) in rats resulted in a sustained 70-mmHg rise in blood pressure during 7 days of treatment. A marked dipsogenic response preceded the maximal rise in blood pressure, peaked at 24 h, and returned to control by the 5th day. Urinary sodium excretion rose on the 1st day of infusion but thereafter was not different from that of vehicle-infused rats. ANG II-infused rats showed a small but significant kaliuresis, a fall in serum osmolality (5.5 mosmol/kg), but no change in plasma Na+, K+, or glucose. Rats infused with the same dose of ANG II intravenously showed a small, 8-mmHg rise in blood pressure, but none of the changes noted after icv ANG II. Plasma renin activity was suppressed in rats infused with ANG II by both routes. We conclude that the pressor, dipsogenic, and renal excretory effects of icv ANG II are mediated centrally and cannot be explained by leakage of the peptide into the systemic circulation. Furthermore, the pressor and dipsogenic effects of ANG II become clearly dissociated during chronic icv infusion.

Angiotensin II↗
PubMed1982

A comparison of inhibition of angiotensin I conversion by three converting enzyme inhibitors in rats.

1. The pressor responses to angiotensin I (AI) were suppressed in a dose related manner by the three converting enzyme inhibitors (CEI); SA 446, SQ 14 225 and MK 421. 2. The inhibitory action of SA 446 and SQ 14 225 was rapid in onset and decayed with time, while that of MK 421 was slower in onset and maintained for the 1 h of observation. 3. A single oral administration of MK 421 (80 mumol/kg) significantly decreased the pressor effect of AI 24 h later. In contrast, neither SA 446 nor SQ 14 225 reduced the AI-induced response at this time. 4. In anaesthetized genetically hypertensive rats, the depressor effect of MK 421 was greater than that of either SA 446 or SQ 14 225.

3-Mercaptopropionic Acid↗
PubMed1981

Solubilization of immune precipitates by six isolated alternative pathway proteins.

Immune precipitates were solubilized by the alternative pathway of complement assembled from isolated proteins, i.e., C3, factor B, factor D, properdin, C3b inactivator (C3bINA), and beta 1H. The kinetic curves of solubilization in the isolated system and in EGTA-serum were virtually indistinguishable. No requirement of other factors was apparent. Deletion of C3bINA and beta 1H from the complete mixture caused total consumption of C3 in the fluid phase and resulted in neither C3 binding to the complexes nor solubilization. Thus, the presence of a regulated fluid-phase reaction is essential for efficient fixation of C3 and the consequent solubilization. In addition, properdin plays an essential role in the complement-mediated solubilization in the presence of the two regulators. A large amount of C3 was incorporated into the antigen-antibody lattice. Solubilization of immune complexes started after the binding of one C3 molecule to one antibody molecule in the complexes, and the molar ratio of C3:antibody in the solubilized complexes also is approximately 1.

Animals↗
PubMed1981

S-Adenosylhomocysteine hydrolase from rat liver. Purification and some properties.

S-Adenosylhomocysteine hydrolase (EC 3.3.1.1) from rat liver was purified to homogeneity. The enzyme had a molecular weight of 188,000 and was composed of 4 subunits with a molecular weight of 47,000. The isoelectric pH of the enzyme was at 5.7. The Km values for S-adenosyl-L-homocysteine, adenosine, and DL-homocysteine were 15.2 microM, 1.05 microM, and 155 microM, respectively, at pH 7.2 and 25 degrees C. The enzyme showed a fluorescence with an emission maximum at 350 nm when excited at 280 nm. The protein fluorescence was partially quenched on addition of adenosine. The fluorescence quenching as a function of adenosine concentration indicated that the enzyme contained four binding sites for adenosine per molecule. The same data provided a value of 0.63 microM for the dissociation constant of adenosine. The enzyme possessed 4 mol of tightly bound NAD+/mol. The addition of adenosine to the enzyme caused the appearance of a peak at 327 nm in a concentration-dependent manner. The enzyme-bound NAD+ readily formed an adduct with bisulfite with the concomitant loss of enzyme activity. These data suggest that the bound NAD+ is involved in the catalytic mechanism of the enzyme.

Amino Acids↗
PubMed1981

Role of arginine residue in saccharopine dehydrogenase (L-lysine forming) from baker's yeast.

The baker's yeast saccharopine dehydrogenase (EC 1.5.1.7) was inactivated by 2,3-butanedione following pseudo-first-order reaction kinetics. The pseudo-first-order rate constant for inactivation was linearly related to the butanedione concentration, and a value of 7.5 M-1 min-1 was obtained for the second-order rate constant at pH 8.0 and 25 degrees C. Amino acid analysis of the inactivated enzyme revealed that arginine was the only amino acid residue affected. Although as many as eight arginine residues were lost on prolonged incubation with butanedione, only one residue appears to be essential for activity. The modification resulted in the change in Vmax, but not in Km, values for substrates. The inactivation by butanedione was substantially protected by L-leucine, a competitive analogue of substrate lysine, in the presence of reduced nicotinamide adenine dinucleotide (NADH) and alpha-ketoglutarate. Since leucine binds only to the enzyme-NADH-alpha-ketoglutarate complex, the result suggests that an arginine residue located near the binding site for the amino acid substrate is modified. Titration with leucine showed that the reaction of butanedione also took place with the enzyme-NADH-alpha-ketoglutarate-leucine complex more slowly than with the free enzyme. The binding study indicated that the inactivated enzyme still retained the capacity to bind leucine, although the affinity appeared to be somewhat decreased. From these results it is concluded that an arginine residue essential for activity is involved in the catalytic reaction rather than in the binding of the coenzyme and substrates.

Amino Acids↗
PubMed1980

The inactivation of saccharopine dehydrogenase (L-lysine-forming) by diethyl pyrocarbonate.

Saccharopine dehydrogenase (epsilon-N-(L-glutaryl-2)-L-lysine: NAD oxidoreductase (L-lysine-forming) EC 1.5.1.7) from baker's yeast is inactivated by diethyl pyrocarbonate. Spectrophotometric studies show that the inactivation results from the modification of 3 histidyl residues/molecule of enzyme. The sulfhydryl content of the enzyme is unchanged by modification. The reversibility of inactivation by hydroxylamine and the pH dependence of inactivation are also consistent with the inactivation being due to modification of the histidyl residue. Although the coenzyme and substrates are without effect when added singly, the inactivation is completely protected by alpha-ketoglutarate in the presence of a saturating concentration of NADH. Since alpha-ketoglutarate binds only to the enzyme . NADH complex, the results suggest that the inactivation is due to modification of the residue at or near the substrate-binding site. Under the conditions where the inactivation is largely protected by NADH plus alpha-ketoglutarate, 2 histidyl residues appear to be modified suggesting that only 1 residue involved in the catalytic activity. The modification appears to prevent the binding of alpha-ketoglutarate, but not of the coenzyme, to the enzyme. The protein fluorescence of the native and modified enzymes is quenched by NAD+ and NADH. However, the NADH titration curve of the modified enzyme is not affected by alpha-ketoglutarate, in contrast to the native enzyme which shows an increase in the apparent affinity for the coenzyme in the presence of alpha-ketoglutarate.

Binding Sites↗
PubMed1980

Regional differences in electrical and mechanical properties of guinea-pig mesenteric vessels.

Regional differences in electrical and mechanical properties of guinea-pig mesenteric vessels were investigated using microelectrode and isometric tension recording methods. The amplitude of membrane potentials differed according to region and in the following order; branch of jejunal artery (BJA) > cranial mesenteric artery (CMA) > jejunal artery (JA) greater than or equal to jejunal vein (JV) not equal to portal vein (PV). There were also regional differences in the muscle membrane potential with various concentrations of [K]o or [Na]o, while no differences were observed with applications of various concentrations of [Ca]o or [Cl]o. ACh produced hyperpolarization of the muscle membrane in the CMA, JA and JV but not in the PV and BJA. Hyperpolarization in the JA mainly followed increase in the K-permeability, and a reversal potential for ACh was distributed at about -70mV. In the JV, the ACh-induced hyperpolarization accompanied tension development. Phenylephrine depolarized the muscle membranes of the CMA, JA and PV but not of the BJA and JV. Low concentrations of phenylephrine produced contractions with no depolarization of the membrane in the JA and CMA. Isoprenaline-induced hyperpolarization was smaller in arteries than in veins, and this hyperpolarization was reduced in amplitude with repeated applications. The ACh-induced relaxation and phenylephrine-induced contraction were larger in the JA than in the CMA. Regional differences of the muscle property in response to application of different agents were discussed in relation to the physiological roles.

Animals↗
PubMed1979

Stereospecificity of hydrogen transfer in the saccharopine dehydrogenase reaction.

The stereospecificity of hydrogen transfer in the synthesis of saccharopine from alpha-ketoglutarate and L-lysine catalyzed by saccharopine dehydrogenase (N5-(1,3-dicarboxypropyl)-L-lysine: NAD oxidoreductase (L-lysine-forming), EC 1.5.1.7) was examined by using [4A-3H]- and [4B-3H]NADH. The enzyme showed the A-stereospecificity. The NMR analysis of the saccharopine prepared with [4"A-2H]NADH revealed that the label was incorporated into the C-2 of the glutaryl moiety.

Hydrogen↗