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Biomedical subjects

A Baba

Publications and source records attributed to A Baba.

At least 253 records · Page 14Linked to original sources
PubMed1987

Intracellular free calcium concentration, Ca++ channel and calmodulin level in experimental hypertension in rats.

Using fluorescent calcium indicator quin2, we studied intracellular free calcium concentration in platelets that have a number of features similar to vascular smooth muscle cells. Intracellular free calcium concentration in platelets of male SHR was significantly higher at 4, 11 and 28 weeks old compared with age-matched male WKY. However, no significant difference was observed in platelets cytosolic free calcium level of DOCA-salt hypertensive and two-kidney, one clip hypertensive rats in the chronic stage. Cardiac Ca++ channels were estimated by means of radioligand binding method with [3H]-nimodipine. No significant changes were observed in the concentration and affinity of cardiac Ca++ channel in SHR, DOCA-salt hypertensive and two-kidney, one clip hypertensive rats. Calmodulin levels in mesenteric arteries of SHR were significantly decreased in comparison with those of WKY. However no significant differences were observed in DOCA-salt hypertensive rats in the chronic stage. These results indicate that the increase in intracellular free calcium concentration of SHR is not the secondary change caused by high blood pressure. It is impossible to detect the ratio of the three states (open, resting and inactivated) of Ca++ channel. Therefore, there remains a possibility of the changes in the ratio of the states of Ca++ channel. The observed abnormalities of Ca++ regulation may contribute to the pathogenesis of hypertension.

Animals↗
PubMed1987

Neurochemical characterization of cysteine sulfinic acid, an excitatory amino acid, in hippocampus.

In this communication, I have summarized our studies on the possible roles of cysteine sulfinic acid (CSA) in the central nervous system (CNS), from these observations, CSA was suggested to be a neurotransmitter. We reported the presence of CSA in the CNS and subsequently characterized Na+-dependent high affinity uptake and depolarization-induced release of CSA. Depolarization-induced release of [14C]CSA from the preloaded hippocampal slices was specifically attenuated by benzodiazepines and GABA agonists. Synaptic membranes have a Na+-dependent specific binding site for cysteic acid, an analogue of CSA, which may be a possible binding site for CSA. This binding site seemed to be distinct from that for glutamate. To assess CSA as a physiologically active candidate which is distinct from glutamate, two neurochemical experiments were performed: one experiment determined the enhancement by excitatory amino acids of depolarization-induced release of [3H]GABA from the preloaded slices, and the other one monitored the cyclic AMP formation by excitatory amino acids in hippocampal slices. In both studies, differences in the responses to the various antagonists indicate that CSA receptors are distinct from glutamate receptors. Furthermore, we proposed that excitatory amino acid receptors which are subsequently linked to adenylate cyclase are functionally related to the Cl- channel.

Amino Acids↗
PubMed1987

Effect of 5-(3-[4-(4-fluorophenyl)-1-piperazinyl]-propoxy)indan (BP-528) on benzodiazepine receptor bindings and gamma-aminobutyric acid release.

The action of a new type of anti-anxiety compound, 5-(3-[4-(4-fluorophenyl)-1-piperazinyl]-propoxy)indan (BP-528), was tested on benzodiazepine receptor bindings and on [3H]-GABA release. BP-528 did not alter [3H]-diazepam binding to rat cerebral cortical and hippocampal membranes either in the presence or absence of GABA; and the binding of [3H]-propyl-beta-carboline-3-carboxylate at low concentration (0.04 nM), which labels only the type I benzodiazepine receptor, was not changed by BP-528. BP-528 did not interact with the GABA-benzodiazepine receptor complex, which is related to the anti-anxiety activity of benzodiazepines. This compound affected neither GABA binding nor GABA uptake. Ten micromolar BP-528 depressed high K+-induced [3H]-GABA release from preloaded rat hippocampal slices. However, the same concentration of BP-528 also inhibited high K+-induced calcium uptake by rat cerebral cortical synaptosomes.

Animals↗
PubMed1987

Effects of nicardipine on blood pressure and platelet cytosolic free calcium concentration in SHR.

Intracellular free calcium concentration was measured by the fluorescent calcium indicator quin2 method in platelets of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, and the effects of nicardipine on platelet cytosolic free calcium concentration were investigated. Cytosolic free calcium concentration was significantly increased in platelets of 4-, 11-, and 14-week-old SHR compared with age-matched WKY rats. Platelet cytosolic free calcium concentration in 14-week-old male SHR was significantly decreased 1 h after the administration of nicardipine (5 mg/kg p.o.), while that in WKY rats remained unchanged. These results suggest that transmembrane Ca2+ influx is genetically increased in SHR.

Administration, Oral↗
PubMed1987

Ca mobilization from the intracellular Ca store in spontaneously hypertensive rats.

To evaluate the size of the intracellular Ca store in spontaneously hypertensive rats (SHR), caffeine-induced contractions were investigated in mesenteric artery preparation. Twelve-week-old SHR and age-matched Wistar-Kyoto (WKY) rats were used. The isolated mesenteric artery was prepared by the method of McGregor. Caffeine (2 mg)- and norepinephrine (2 micrograms)-induced pressor responses were measured in both normal (Ca, 2 mM) and Ca-free solution (1 mM EGTA solution). In the presence of Ca, pressor responses to exogenous norepinephrine in SHR were higher than those in WKY rats. In Ca-free solution, pressor responses to norepinephrine were markedly reduced in SHR compared to WKY rats and caffeine-induced contractions in SHR were lower than those in WKY rats. These results suggest that pressor responses to norepinephrine in SHR may be more dependent on extracellular Ca than in WKY rats and the caffeine-sensitive intracellular Ca store might be less in SHR.

Animals↗
PubMed1986

Assay of phospholipase A2 activity of synaptic membranes using a phospholipid transfer protein: stimulation by depolarization.

A phospholipid transfer protein from bovine liver was used to transfer exogenous ([14C]linoleoylphosphatidylethanolamine [14C]linoleoyl PE) into synaptic membranes and synaptosomes without modifying the lipid compositions in order to study the intrinsic activity of phospholipase A2 of the preparations. Results were compared with the conventional method in which the substrate was simply dispersed with the enzyme preparations. Liberation of [14C]linoleic acid from [14C]linoleoyl PE-preloaded synaptic membranes by the transfer protein continued almost linearly over 60 min of incubation in the presence of Ca2+. The dose-response curve of Ca2+ for the activity of phospholipase A2 obtained in the present method was slightly shifted to the left in comparison with the conventional method: Ca2+ even at the concentration of 100 microM significantly enhanced the enzyme activity. Requirement of Ca2+ for the reaction is more specific in the present method than in the conventional one. When synaptosomes were prelabeled with [14C]linoleoyl PE by the transfer protein, the liberation of [14C]linoleic acid during the incubation at 37 degrees C increased linearly over 2 min. The liberation of [14C]linoleic acid was significantly enhanced in the presence of 56 mM KCl, 50 microM veratridine and 50 microM calcium ionophore A23187. These agents did not stimulate the reaction in the absence of Ca2+.

Animals↗
PubMed1986

Monocyte activating factor in sarcoidosis. I. Existence of the factor in sarcoidosis sera.

Sarcoidosis sera were found to have the ability to induce normal human monocytes to spread. Gel filtration of sarcoidosis sera on Sephadex G-200 showed that the factor mainly responsible for this activity had a molecular weight of about 70,000. The spreading factor also possessed the ability to increase all cell size of normal human monocytes as well as to increase their phagocytosis and glucose consumption. Accordingly, the spreading factor seems to be considered as a monocyte activating factor. Sarcoidosis sera showed a macrophage migration inhibitory activity, as well. On Sephadex G-200 column chromatography of the sera, the most obvious inhibitory activity was eluted in the fraction with a molecular weight of about 45,000. The macrophage migration inhibitory factor had the ability neither to increase cell size of normal human monocytes nor to increase their phagocytosis and glucose consumption.

Blood Glucose↗
PubMed1986

Monocyte activating factor in sarcoidosis. II. Secretion of the factor from monocytes.

The normal human monocytes pretreated with the monocyte activating factor found in sarcoidosis sera were shown to secrete a factor which induced normal human monocytes to spread as well as to increase their cell size. Phagocytosis and glucose consumption of normal human monocytes were also increased by this secondarily obtained factor. Its molecular weight was about 70,000. These results indicate that this secondary factor may be the same substance as the monocyte activating factor found in sarcoidosis sera. The normal human monocytes pretreated with the monocyte activating factor were also shown to liberate a factor which generated macrophage migration inhibitory factor in cooperation with normal human sera.

Animals↗
PubMed1986

Chemical modification and fluorescence labeling study of Ca2+,Mg2+-adenosine triphosphatase of sarcoplasmic reticulum using iodoacetamide and its N-substituted derivatives.

Sarcoplasmic reticulum membrane vesicles from rabbit skeletal muscle were treated with iodoacetamide (IAA) at pH 7.0 and 30 degrees C. At 1.0 mM IAA, 1 mol of IAA per mol of ATPase peptide was bound in 1 h. Under these conditions, IAA was attached specifically to the B-tryptic fragment portion of the peptide. The binding of IAA did not affect the Ca2+-transporting activity of ATPase. Three fluorescent derivatives of iodoacetamide, 5-(2-acetamidoethyl)aminonaphthalene-1-sulfonate (IAEDANS), 5-iodoacetamido fluorescein (IAF), and 5-iodoacetamido eosin (IAE), were also tested for reactivity toward sarcoplasmic reticulum ATPase at 30 degrees C and pH 7.0. In 1 h at 50 microM concentration, each of these fluorescent labels modified ATPase to a labeling density of 1 mol per mol of ATPase. Neither IAEDANS nor IAF at this labeling density affected Ca2+-transporting activity, but IAE reduced it to 20% of the untreated control. The target site of IAEDANS at this labeling density was located exclusively on the B-fragment portion, as was the case with IAA, but IAF label was found on both A1 and B fragments after limited tryptic digestion. IAEDANS was used as a B-fragment portion-directed conformational probe of Ca2+-transport ATPase, and an increase in fluorescence intensity accompanying E1Ca-P formation was detected. The fluorescence enhancement was abolished when E1Ca-P X ADP beta S was formed by adding ADP beta S to preformed E1Ca-P. This suggests that the conformation of ATPase in the neighborhood of the IAEDANS binding site may be altered in response to the dissociation of ADP from the phosphorylated intermediate.

Adenosine Diphosphate↗
PubMed1986

Regulation of taurine transport in rat skeletal muscle.

Taurine concentration of soleus muscle (SL, slow-twitch) was initially about twofold higher than that of extensor digitorum longus muscle (EDL, fast-twitch). Taurine concentration in gastrocnemius muscle (GC) was intermediate between that of EDL and SL. Four days after sciatic nerve section, taurine concentration in the EDL but not in the SL was increased by 2.5-fold. The increase was not due to the muscle atrophy and was observed 28 days after denervation. Tenotomy did not increase the total taurine content of the EDL. The increase in taurine concentration of the denervated EDL was prevented by simultaneous ingestion of guanidinoethane sulfonate, a competitive inhibitor of taurine transport. The initial and the maximal rates of [3H]taurine uptake were significantly higher in SL than in EDL. Denervation dramatically accelerated the initial and the maximal rates of the transport in EDL, whereas it significantly reduced those in SL. In contrast, the electrical stimulation of sciatic nerve accelerated the uptake of taurine by EDL and SL of the control but not of the curare-treated rats. These results suggest that transport of taurine into rat skeletal muscles is regulated differently by neural information and by muscular activity, and that the regulation is dependent on the muscle phenotype.

Animals↗
PubMed1986

Stimulatory effect of veratridine on lysophosphatidylethanolamine formation in rat brain synaptosomes.

[3H]-Arachidonic acid incorporation into phospholipids of synaptosomal lysates prepared from veratridine-treated synaptosomes was examined. Synaptosomal lysates were shown to acylate exogenously added lysophosphatidylcholine, lysophosphatidylinositol, and lysophosphatidylethanolamine, when incubated with [3H]-arachidonic acid, ATP, CoA and MgCl2, yielding the respective phospholipids. Preincubation of synaptosomes with veratridine for 30 sec gave rise to an increase in [3H]-arachidonic acid incorporation into phosphatidylethanolamine, but not phosphatidylcholine nor phosphatidylinositol, indicating that lysophosphatidylethanolamine might be produced by veratridine. This increase of radioactivity in phosphatidylethanolamine caused by veratridine was completely inhibited by 1 microM tetrodotoxin or in calcium-free condition. These observations show that lysophosphatidylethanolamine was formed in a calcium-dependent manner and accumulated in synaptosomes treated with veratridine, which may relate to its action on the sodium channel and enhanced calcium influx.

Animals↗
PubMed1986

Taurine transport in chronically stimulated fast- and slow-twitch muscles of the rat.

Indirect stimulation via the sciatic nerve, 10 or 100 Hz stimulus trains of 1 sec duration, applied every 3 sec, 8 hr/day for 1-4 weeks increased taurine concentration of the extensor digitorum longus (EDL, fast-twitch) muscle of the rat. The uptake of [3H]-taurine into the EDL and tibialis anterior (TA, fast-twitch) muscle was also increased by the stimulation. Concentration and uptake of taurine in the soleus muscle (SL, slow-twitch) did not change by chronic 10 Hz stimulation. Taurine concentration in the SL muscle was significantly reduced by chronic 100 Hz stimulation. This study shows that chronic nerve stimulation increases the uptake of taurine in the fast-twitch muscles, but not in the slow-twitch muscle.

Animals↗
PubMed1985

Membrane-bound lipoxygenase of rat cerebral microvessels.

The microvessels isolated from rat cerebral cortex has arachidonate lipoxygenase activity, which was not due to possible contamination of the platelets. The major product was identified to be 12-hydroxyeicosatetraenoic acid. After homogenization and sonication of the microvessel preparations, the lipoxygenase activity was recovered both in the membrane- and the cytosol-fractions, whereas that in the platelets was recovered in the cytosol fraction. Membrane-bound lipoxygenase of the microvessels has apparent Km value of 3.8 microM for arachidonic acid, which was corresponded to 1/5 of that in the platelet enzyme. Microvessel lipoxygenase was inhibited by nordihydroguaiaretic acid but not by indomethacin.

Animals↗