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Biomedical subjects

A Baba

Publications and source records attributed to A Baba.

At least 235 records · Page 13Linked to original sources

Calcium induces membrane translocation of 12-lipoxygenase in rat platelets.

Translocation of soluble 12-lipoxygenase to membranes was examined in rat platelets. Preincubation of platelet homogenates with 0.1-10 microM Ca2+ resulted in an increase in 12-lipoxygenase activity of the particulate fraction with a concomitant decrease in that of the soluble fraction. Kinetic parameters of 12-lipoxygenase of the soluble and membrane fractions were not changes in the presence of 10 microM Ca2+. Ca2+-induced association of 12-lipoxygenase to the particulate fraction was dependent on the amounts of platelet-soluble and membrane fractions but not on the incubation temperature. 12-Lipoxygenase activity associated with the particulate fraction was completely dissociated by reducing the concentration of Ca2+ to 10 nM. Ca2+-induced association of the enzyme also occurred in the boiled- and trypsin-treated membranes but was significantly reduced in the phospholipase A2-treated membranes. Soluble 12-lipoxygenase also associated to liposomes in a Ca2+-dependent manner. Pretreatment of platelets with thrombin (0.5-5 units/ml) significantly caused a translocation of soluble 12-lipoxygenase to particulate fraction; in the time course study, the translocation was observed at the thrombin pretreatment of 1, 5, and 10 min. These results suggest that stimulation of platelets is followed by the translocation of soluble 12-lipoxygenase to membranes, which is mediated by physiological concentration of Ca2+.

Animals↗

L-[35S]cysteic acid selectively detects chloride-dependent L-glutamate transporters in synaptic membrane.

Na+-independent L-[35S]cysteic acid (CA) accumulation in rat cortical synaptic membrane was examined. In the absence of Cl-, the accumulation was not observed. Addition of Cl- revealed the accumulation in a dose-dependent manner. Br- and NO3- also did. Ca2+-enhanced the Cl- -dependent accumulation, whereas low concentrations of Na+ reduced it. L-[35S]CA accumulation was inhibited by quisqualate, L-glutamate (L-Glu), L-cysteine sulfinate, D,L-homocysteic acid and D,L-2-amino-4-phosphonobutyrate (D,L-APB) potently. L-CA inhibited L-[3H]Glu accumulation in synaptic membrane in the presence of Cl-. The maximal inhibition of L-CA was equal to that of D,L-APB, but L-CA did not inhibit L-[3H]Glu accumulation in the absence of Cl-. These results show that L-[35S]CA selectively detects the Cl- -dependent L-Glu transporters in synaptic membrane.

Amino Acids, Sulfur↗

Excitatory amino acids enhance dissociation of zinc from soluble protein in cytosol of rat hippocampus.

An ultra-filtration method for separating free Zn from its bound form with macromolecules was used to study the effect of excitatory amino acids on dissociation of Zn in the soluble fraction of rat hippocampus. L-Glutamate, L-aspartate and L-cysteic acid but not D-glutamate significantly increased the dissociated Zn at the concentration of 100 microM. 2-Amino-5-phosphonovalerate did not inhibit the effect of L-glutamate. Likewise, the stimulatory effect of N-methyl-DL-aspartate and quisqualate was observed at the concentration range between 1 and 100 microM. The effect of kainate was much less potent. Taurine and GABA had no stimulatory effect on the dissociation of Zn.

Amino Acids↗

Difference in thiamine metabolism between extensor digitorum longus and soleus muscles.

1. Thiamine diphosphate level was higher in soleus muscle than in extensor digitorum longus muscle in various animals, whereas thiamine triphosphate level was less in the former muscle than in the latter except for mouse. 2. 2-Oxoglutarate dehydrogenase, transketolase and thiamine pyrophosphokinase activities were higher in soleus muscle than in extensor digitorum longus in rat and guinea pig. 3. The differences between rat two muscle phenotypes in thiamine diphosphate, but not thiamine triphosphate, level and the thiamine-related enzyme activities disappeared after denervation. 4. Tenotomy had little effect on thiamine phosphate levels and the thiamine-related enzyme activities in rat skeletal muscles.

Animals↗

Tissue difference in cellular localization of thiamine phosphate esters.

1. Thiamine phosphate levels were determined in the soluble and particulate fractions of various rat tissues. 2. There was marked tissue difference in the cellular localization of thiamine phosphates. 3. Brain thiamine triphosphate was localized only in the particulate fraction, whereas skeletal muscle thiamine triphosphate was in the soluble fraction as a protein-unbound form.

Animals↗

Inhibition by taurine of Na(+)-Ca2+ exchange in sarcolemmal membrane vesicles from bovine and guinea pig hearts.

1. Taurine, but not GABA, beta-alanine and glycine, inhibited Na(+)-dependent Ca2+ uptake in bovine cardiac sarcolemmal membrane vesicles in a dose-dependent manner. 2. The inhibition of Na(+)-dependent Ca2+ uptake was noncompetitive with respect to Ca2+ concentration. 3. The inhibitory effect of taurine on the exchange was also observed in cardiac sarcolemmal vesicles prepared from guinea pig, but not from rat. 4. Taurine did not affect Na(+)-dependent Ca2+ efflux nor ATP-dependent Ca2+ uptake in the bovine cardiac membranes.

Adenosine Triphosphate↗

Inherited deficiency of the seventh component of complement: studies of C7-consuming activity.

Neither the hemolytic activity nor the protein level of the seventh component of serum complement (C7) was detectable in an 8-year-old girl with nephritis, but in her parents and her brother, they were about half of the normal level. The patient was a homozygote type with a complete deficiency of C7 while her parents and brother were all heterozygote type with a partial deficiency of C7. C7-consuming activity was demonstrated in the native serum of the patient with complete C7 deficiency, and it was found that large amounts of C56 were readily generated upon incubation of the patient's serum with zymosan. It is proposed that the C7-consuming activity in the native serum of this patient is due to small amounts of C56 generated during the activation of serum complement by some kind of infection such as a common cold.

Child↗

Postnatal development of thiamine metabolism in rat brain.

The activities of thiamine diphosphatase (TDPase), thiamine triphosphatase (TTPase), and thiamine pyrophosphokinase and the contents of thiamine and its phosphate esters were determined in rat brain cortex, cerebellum, and liver from birth to adulthood. Microsomal TTPase activity in the cerebral cortex and cerebellum increased from birth to 3 weeks, whereas that in the liver did not change during postnatal development. Microsomal TDPase activity in the cerebral cortex showed a transient increase at 1-2 weeks, but that in the cerebellum did not change during development. In contrast to the activity of the brain enzyme, that of liver microsomal TDPase increased stepwise after birth. Thiamine pyrophosphokinase activity in the cerebellum increased from birth to 3 weeks and then decreased, whereas that in the cerebral cortex and liver showed less change during development. TDP and thiamine monophosphate (TMP) levels increased after birth and plateaued at 3 weeks whereas TTP and thiamine levels showed little change during development in the cerebral cortex and cerebellum. The contents of thiamine and its phosphate esters in the liver showed more complicated changes during development. It is concluded that thiamine metabolism in the brain changes during postnatal development in a different way from that in the liver and that the development of thiamine metabolism differs among brain regions.

Acid Anhydride Hydrolases↗

Depolarization increases chloride-dependent glutamate sequestration in synaptic membranes of rat cerebral cortex.

To assess the functions of Cl- -dependent glutamate "binding" (Cl- -dependent glutamate uptake) in synaptic membranes, possible effects of depolarization on the uptake were examined. When rat cerebral cortical slices were preincubated with depolarizing agents such as veratrine (7 micrograms/ml), 10 microM aconitine, 56 mM K+, and 50 microM monensin, [3H]glutamate uptake by the crude synaptic membranes, which were subsequently prepared from the pretreated slices, was increased by 60-85%. Stimulation of the glutamate uptake by predepolarization was dependent on Na+ but not on Ca2+. The bindings of gamma-[3H]aminobutyric acid and 5-[3H]hydroxytryptamine were not significantly affected by the predepolarization. Veratrine pretreatment increased the maximal density of the glutamate uptake sites without affecting the affinity for glutamate. Several characteristics of the uptake sites increased by the veratrine pretreatment coincided with those of Cl- -dependent glutamate uptake sites. Na+-dependent glutamate binding (Na+-dependent glutamate uptake) to the membranes was not affected by pretreatment with veratrine. The content of endogenous glutamate and the noninulin space in the membrane fractions were not changed by the predepolarization. The increase in the glutamate uptake induced by pretreatment with high K+ was reversible: it returned to the control level after a second incubation of the slices in control medium. These results suggest that the Cl- -dependent glutamate sequestration system in synaptic membranes is regulated by the membrane potential.

Aconitine↗

Blood pressure and sympathetic activity following responses to aerobic exercise in patients with essential hypertension.

Fourteen untreated patients with essential hypertension (EH) were subjected to mild aerobic exercise with the intensity at 50% of the maximum oxygen uptake (VO2max) twice a week for 12 weeks, as compared with 14 normotensive subjects (NT). Blood pressure and norepinephrine (NE) in plasma, platelet and urine were measured as the indices of sympathetic activity. In EH, a significant fall in both systolic and diastolic blood pressure was observed. In addition, exercise training produced a significant decrease both urinary and platelet NE, but not in plasma NE. Neither significant changes in blood pressure nor NE in plasma, platelet and urine were observed in NT. These results suggest that an inhibition of the sympathetic nervous system might be related to the blood pressure fall in physical exercise training.

Adult↗

[Contribution of calmodulin to renin release in spontaneously hypertensive rats].

A comparative study was designed to evaluate the contribution of calmodulin to renin release from isolated glomeruli of spontaneously hypertensive rats (SHR, Okamoto and Aoki). Male 7-week-old SHR and age-matched control Wistar-Kyoto rat (WKY) were used in the present study. Glomeruli were isolated by the method of Beierwaltes et al. Isolated glomeruli were placed within the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 ml/minute at 37 degrees C. Renin release was increased by calmodulin inhibitor, W-7 in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 compared to WKY. This result indicates that calmodulin plays an inhibitory role in renin release from juxtaglomerular cells. Calmodulin-mediated suppression mechanism in renin release is augmented in SHR.

Animals↗

Increased concentration of calcium channel and intracellular free calcium in the acute phase of deoxycorticosterone acetate salt hypertension.

Cardiac calcium channels and platelet Ca2+ concentrations were examined in deoxycorticosterone acetate (DOCA)-salt hypertension in rats to clarify the role of calcium channels in the regulation of intracellular Ca2+. Calcium channels were determined by the radioligand binding method and platelet Ca2+ concentrations were measured by a fluorescent Ca2+ indicator, Quin-2. The number of cardiac calcium channels was increased in DOCA-salt hypertension compared with controls 10 days after nephrectomy. Platelet Ca2+ concentrations were also increased in the acute phase of DOCA-salt hypertension. No significant changes were observed in the number of cardiac calcium channels and in platelet Ca2+ concentrations in the chronic phase of DOCA-salt hypertension. These results suggest that the increased platelet Ca2+ concentrations are induced by the increase in the number of calcium channels in the acute phase of hypertension.

5'-Nucleotidase↗

Inhibition by forskolin of excitatory amino acid-induced accumulation of cyclic AMP in guinea pig hippocampal slices.

The effect of forskolin on the excitatory amino acid-induced accumulation of cyclic AMP was examined in hippocampal preparations of the guinea pig. Forskolin at concentrations of 0.1-10 microM remarkably enhanced the stimulatory effects of histamine and adenosine, whereas it markedly attenuated the stimulation induced by cysteine sulfinate, an excitatory amino acid. Forskolin reduced the maximal response to cysteine sulfinate without affecting the apparent ED50. At a concentration of 1 microM, forskolin also inhibited the stimulatory effects of glutamate, N-methyl-DL-aspartate, and veratridine without affecting those of kainate and quisqualate. Pretreatment of the slices with 0.1 mM N-ethylmaleimide partially prevented the attenuation by forskolin of cysteine sulfinate-induced accumulation of cyclic AMP without affecting the stimulation induced by cysteine sulfinate. Forskolin at concentrations of less than 1 microM did not affect GTP-stimulated activity and Cl- -dependent activity of adenylate cyclase of the hippocampal membranes.

Adenosine↗

Mechanism of excitatory amino acid-induced accumulation of cyclic AMP in hippocampal slices: role of extracellular chloride.

We show the involvement of chloride transport on excitatory amino acids-induced accumulation of cyclic AMP in brain slices. The stimulation of cyclic AMP formation induced by excitatory amino acids in guinea pig hippocampal slices was absolutely dependent on the presence of Cl- in the incubation medium. The apparent half-maximal concentration of chloride was about 30 to 40 mM with the maximum response at more than 60 mM. As regards to the anion selectivity for the stimulation by excitatory amino acids, Br- was fully effective as Cl-, whereas F- and SO42- were ineffective. DL-(+/-)-2-Amino-4-phosphonobutyric acid, an antagonist of excitatory amino acid receptors, reduced significantly the response to excitatory amino acids. In the Cl- -free medium, the stimulatory effects of 50 microM veratridine, 10 microM forskolin and 100 microM histamine were reduced markedly but still significantly observed. The anion exchange blockers at the concentrations of more than 1 mM reduced significantly the cyclic AMP formation induced by an excitatory amino acid in a dose-dependent manner. Furosemide at the concentration of 3 mM negated the Cl- -dependent responses to forskolin and histamine without affecting the Cl- -independent ones. Furosemide did not inhibit the adenylate cyclase activity of hippocampal synaptic membrane fractions.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗