Biomedical subjects

A Baba

Publications and source records attributed to A Baba.

At least 37 records · Page 2Linked to original sources

PubMed1991

Gonadal hormones affect the hypothermia induced by serotonin1A (5-HT1A) receptor activation.

Subcutaneous injection of 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) in mice caused hypothermia which was antagonized by pindolol. The hypothermic effect of 8-OH-DPAT was pronounced in female than in male mice. The sex difference in the hypothermic effect was also observed after pretreatment with proadifen. The hypothermic effect of 8-OH-DPAT was attenuated by ovariectomy. In the ovariectomized mice, the effect of 8-OH-DPAT on rectal temperature was enhanced by chronic estradiol and the enhancement was blocked by simultaneous administration of testosterone. In male mice the hypothermic effect of 8-OH-DPAT was enhanced by castration. These results suggest that gonadal hormones affect the 5-HT1A receptor-mediated response.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1991

Ramsay Hunt syndrome with mental disorder.

This is a case of Ramsay Hunt syndrome with mental disorder. The patient had action myoclonus, grand mal seizure and severe cerebellar ataxia. Schizophrenia-like symptoms including delusion of persecution and self-reference, auditory hallucination and incoherence were characteristically observed before the neurological disturbance became manifest. Subsequently, euphoria, disinhibition, moria and mild dementia appeared with neurological symptoms. The possibility of Ramsay Hunt syndrome to accompany organic mental syndromes and the relationship between cerebellar dysfunction and psychiatric symptoms are discussed.

Adult↗

PubMed1991

Antihypertensive effects of oral calcium supplementation in spontaneously hypertensive rats.

This study was designed to clarify the mechanisms underlying the antihypertensive action of oral calcium supplementation in SHR. Four-week-old SHR and age-matched WKY were divided into calcium-supplemented and control groups. Calcium supplementation was carried out by giving 1.2% CaCl2 solution as drinking water ad libitum. Distilled water was given to the control group. After 3 weeks of treatment, plasma NE, pressor response to NE in isolated mesenteric artery, platelet cytosolic free calcium concentration and membrane fluidity of erythrocytes were evaluated. The elevation of blood pressure were retarded in calcium supplemented SHR. Calcium supplementation reduced the augmented pressor response to NE and the high level of cytosolic free calcium concentration in SHR. WKY showed no significant changes of these parameters by calcium supplementation. In conclusion, calcium supplementation reduces blood pressure through the reduction of sympathetic and vascular tone in SHR.

Administration, Oral↗

PubMed1991

NMDA induces protein kinase C translocation in guinea pig cerebral synaptoneurosomes.

N-methyl-D-aspartate (NMDA)-induced translocation of protein kinase C from the cytosol to membrane fractions was examined by the [3H]phorbol 12,13-dibutyrate (PDBu) binding method in guinea pig cerebral synaptoneurosomes. Pretreatment of synaptoneurosomes with NMDA, but not that with quisqualate or kainate, induced changes in the distribution of [3H]PDBu binding in the cytosol and membrane fractions in a dose-dependent manner. The NMDA-induced changes of the binding were completely dependent on Ca2+ and inhibited by NMDA receptor antagonists Mg2+, 2-amino-5-phosphonovaleric acid and ketamine, but not by Zn2+. Glycine slightly potentiated the NMDA-induced changes of [3H]PDBu binding. NMDA stimulated Ca2+ uptake but not the phosphoinositide hydrolysis in the synaptoneurosomes. These results suggest that NMDA enhances Ca2+ influx through receptor-operated Ca2+ channels, increasing intracellular calcium concentration and thereby induces translocation of protein kinase C.

Animals↗

PubMed1991

Altered renin release from isolated superfused rat glomeruli in DOCA-salt hypertensive rats.

The present study was designed to clarify the role of calcium in suppressed renin release in DOCA-salt hypertension. Rat glomeruli were isolated by the modified Beierwaltes' sieving method. The glomeruli were superfused with Krebs-Ringer solution. Basal levels of renin release were lower in the DOCA-salt hypertensive rats (1.16 +/- 0.27 ng/ATI/hr/hr/10(4) glomeruli, mean +/- SEM, n = 8) than in the control rats (1.92 +/- 0.18, p less than 0.01, n = 8). Perfusion with a calcium free solution containing EGTA and A23187 stimulated renin release in the DOCA-salt hypertensive and control rats. The maximum levels of renin release during the perfusion in DOCA-salt hypertensive rats (1.79 +/- 0.17, n = 8) were lower than those in control rats (10.60 +/- 1.85, p less than 0.01, n = 8). These results suggest that high levels of intracellular calcium might not contribute to the suppression of renin release in DOCA-salt hypertension.

Animals↗

PubMed1991

[Epidemiological profile of pelvic hydatidosis. 15 cases].

Pelvic genital hydatid disease is rare. It accounts for only 0.9% of hydatidoses and 1.8% of operated adnexial masses. Its clinical signs are often misleading, making the preoperative diagnosis difficult. This diagnosis rests on questioning with particular attention to the socio-professional context and previous history of hydatid disease. Ultrasonography is the first choice examination. Treatment is purely surgical, the best technique being total cystectomy, but the best treatment is prevention.

Adolescent↗

PubMed1990

Decrease of Na(+)-Ca2+ exchange activity by ascorbate in rat brain membrane vesicles.

Na(+)-dependent Ca2+ uptake in rat brain microsomal membrane vesicles was inhibited by preincubating the vesicles with ascorbic acid at 0.1-10 mM. The inhibitory effect of ascorbate was blocked by simultaneous addition of ascorbate oxidase. The decrease in activity was not reversed upon removing the ascorbate. The kinetic study showed that the treatment with ascorbate decreased Bmax without a change in Km for Ca2+. The inhibitory effect by ascorbate was also observed in membrane vesicles derived from osmotically shocked synaptosomes and in reconstituted membrane vesicles. The effect by ascorbate was specific: it did not affect either ATP-dependent Ca2+ uptake in the presence of o-phenanthroline, an inhibitor of lipid peroxidation, or Na(+)-dependent glutamate uptake in the membrane vesicles. The activity of Na(+)-Ca2+ exchange was also decreased by isoascorbic acid, but not by ascorbate 2-sulfate at 1 mM. The treatment with glutathione or 2-mercaptoethanol did not affect the Na(+)-Ca2+ exchange activity, while 1 mM dithiothreitol caused the inhibition which was completely blocked by o-phenanthroline. The effect of ascorbate on Na(+)-dependent Ca2+ uptake was observed even under the conditions which suppress peroxidation of membrane phospholipids.

Animals↗

PubMed1990

An attempt to structurally convert mu-selective morphine toward delta-receptor binding: dimerization based on enkephalin conformation.

In order to elucidate the substrate specificities for mu- and delta-opioid receptors, dimerization of the mu-specific morphine molecule was attempted, based on the hypothesis of the possible relationship between the molecular conformation of endogenous enkephalin and its selectivity for each opioid receptor. The NOR2 ([normorphine]N-CH2-CH2-N[normorphine]) thus synthesized exhibited agonist activity showing a preference for binding with the delta-opioid receptor, compared with the parent morphine molecule. Antagonist activity was also observed for NOR3 ([normorphine]N-CH2-CH2-CH2-N[normorphine]).

Animals↗

PubMed1990

p-chlorophenylalanine attenuates the pituitary-adrenocortical response to 5-HT1A receptor agonists in mice.

The i.p. injection of 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) caused hypothermia and increased the concentrations of serum corticosterone and plasma ACTH in mice. The effects of 8-OH-DPAT at a dose of 2 mg/kg but not of 0.2 mg/kg on the hormone levels were attenuated by pretreatment with p-chlorophenylalanine (pCPA) which depleted brain 5-HT by about 70%; the hypothermic effect of 8-OH-DPAT was, however, not prevented. Similar results were obtained with another 5-HT1A agonist, 1-[3-(3,4-methylenedioxyphenoxy)propyl]-4-phenyl piperazine (BP-554).

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1990

Characteristics of Cl(-)-dependent L-[35S]cysteic acid transport into rat brain synaptic membrane vesicles.

Uptake of L-[35S]cysteic acid (L-CA) in rat synaptic membrane vesicles was investigated. Preincubation with either 10 mM L-glutamic acid (L-Glu), 25 mM L-CA, 10 mM DL-homocysteic acid, or 25 mM DL-2-amino-4-phosphonobutyrate on membrane vesicles enhanced L-[35S]CA and L-[3H]Glu uptake. Na+ (5 mM) and omission of Cl- from the assay medium decreased L-[35S]CA uptake into both 10 mM L-Glu-loaded and non-loaded membrane vesicles. The anion transport blockers, 4-acetamide-4'-isothiocyano-2,2'-disulfonic acid stilbene (SITS) and 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene (DIDS), inhibited L-[35S]CA uptake in a dose-dependent manner. The maximal uptake rate for L-[35S]CA was decreased by 50 microM SITS, while the apparent Km value of L-CA was not changed. SITS increased the EC50 value of Cl- for L-[35S]CA uptake from 5 mM to 10 mM with reduction of the maximal effect. These results suggested that L-[35S]CA uptake into synaptic membrane vesicles was mediated by a SITS-sensitive hetero-exchange transport with non-labeled substrates.

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

PubMed1990

Enhanced DNA synthesis of cultured vascular smooth muscle cells from spontaneously hypertensive rats. Difference of response to growth factor, intracellular free calcium concentration and DNA synthesizing cell cycle.

It is widely reported that cultured vascular smooth muscle cells (CVSMCs) from spontaneously hypertensive rats (SHR) show enhanced proliferation compared with cells from Wistar-Kyoto rats (WKY). The present studies were designed to find out whether this exaggerated proliferation in SHR is determined genetically and, if so, to evaluate the mechanism on the cell cycle. (1) Incorporation of [3H]thymidine into DNA was enhanced in CVSMCs from 3- and 12-week-old SHR compared with WKY but not in CVSMCs from DOCA-salt hypertensive rats compared with the cells from sham-operated rats. (2) DNA synthesis in SHR cells was enhanced further by addition of insulin (which is considered to be a progression factor) but not by arginine-vasopressin (AVP; considered to be a competence factor) or by angiotensin II (AII). On the other hand, insulin, AVP and AII significantly augmented DNA synthesis in WKY cells. (3) Intracellular free calcium concentration was slightly, but significantly, higher in SHR cells. (4) An increase in the population of DNA-synthesizing S-phase cells and decrease in (G2 + M)-phase cells in SHR were observed by flowcytometry. These data suggest (1) that enhanced DNA synthesis in CVSMCs from SHR is determined genetically, (2) that enhanced DNA synthesis in CVSMCs from SHR is largely dependent on an increased proportion of S-phase cells and (3) that this increase in S-phase cells in CVSMCs from SHR could be due to enhanced competence gene expression in SHR cells. (4) The increased intracellular free calcium concentration is compatible with an activation of the inositol-trisphosphate pathway.

Angiotensin II↗

PubMed1990

Deficient activity of nucleotide binding regulatory protein coupled with PGE2 receptor in renal medulla of spontaneously hypertensive rats.

Prostaglandin (PG) E2 receptor-adenylate cyclase system was studied in the kidney of 12-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) to evaluate the role of this system in hypertension. PGE2 receptors were determined by a radioligand binding method using [3H]-PGE2. Adenylate cyclase responses to PGE2, sodium fluoride (NaF) and forskolin were also measured. The concentration of PGE2 receptor was increased in SHR compared with WKY. PGE2- and NaF-stimulated adenylate cyclase activities were significantly lower in SHR than WKY. There was no significant difference in forskolin-stimulated adenylate cyclase activity between SHR and WKY. NaF activates the nucleotide binding regulatory protein (G-protein) and forskolin directly activates the catalytic unit. These results indicate that the activity of G-protein coupled with renal PGE2 receptors is deficient in SHR. This defect may contribute to the elevation of blood pressure, through sodium retention.

Adenylyl Cyclases↗

PubMed1990

Contribution of calmodulin and protein kinase C to renin release in spontaneously hypertensive rats.

This study was designed to evaluate the contribution of calmodulin and protein kinase C 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 rats (WKY) were used in this study. Isolated glomeruli were sealed in the superfusion chamber and perfused with Krebs-Ringer solution at a constant flow of 0.3 mL/min. Renin release was increased by calmodulin inhibitor, W-7, and protein kinase C inhibitor, H-7, in both SHR and WKY. SHR showed higher maximal levels of renin release by W-7 and lower maximal levels by H-7 compared to WKY. These results indicate that calmodulin and protein kinase C play inhibitory roles in renin release from juxtaglomerular cells. The calmodulin-mediated suppression mechanism in renin release appears to be augmented in the SHR, whereas the protein kinase C-mediated system is attenuated.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1990

Responses of cytosolic free calcium to ADP in platelets of spontaneously hypertensive rats.

Abnormalities of Ca2+ handling have been reported in patients with essential hypertension and in spontaneously hypertensive rats (SHR). In this study, responses of cytosolic Ca2+ to ADP in platelets of SHR were examined. Four- and seven-week-old male SHR and age- and sex-matched Wistar-Kyoto rats (WKY) were used. Basal levels of the intracellular Ca2+ concentration in platelets and responses to ADP were estimated using fluorescent indicator fura-2 in the medium containing 1 mmol/L CaCl2 and Ca2(+)-free buffer with 1 mmol/L EGTA. Basal levels of platelet cytosolic Ca2+ of SHR were significantly higher than those of WKY at 4 and 7 weeks of age in the presence of external Ca2+. However, no significant difference was observed in basal levels of platelet cytosolic Ca2+ in the Ca2(+)-free EGTA-containing buffer between SHR and WKY. The peak cytosolic Ca2+ concentration evoked by ADP was significantly diminished in SHR compared with WKY in the absence of external Ca2+, whereas the responses of platelet cytosolic Ca2+ to ADP were similar in SHR and WKY in the presence of external Ca2+. These results suggest that release from intracellular Ca2+ store is reduced in SHR and that the regulation of cytosolic Ca2+ in SHR is more dependent on extracellular Ca2+ compared with WKY.

Animals↗

PubMed1990

Neuropsychiatric disturbances in a patient with a nonmosaic isodicentric (X) (q21.32) chromosome.

A 41-year-old female patient with mental retardation and generalized epileptic seizure had a nonmosaic idic (X) (pter-q21.32::q21.32-pter) chromosome in peripheral lymphocytes and bone marrow cells. Primary amenorrhea, myelodysplastic syndrome, pigmented nevi and characteristic facial appearance were also observed. A few cases with the nonmosaic idic (X) (q::q) with various breakpoints reported previously commonly showed ovarian failure with dysfunction of relevant hormone. CNS abnormalities of the present case were demonstrated by CT, MRI and SPECT using 123I-IMP. CNS abnormalities were considered to be possibly due to karyotype with a nonmosaic idic (X) (q21.32).

Abnormalities, Multiple↗

PubMed1990

Inhibition by ibudilast of leukotriene D4-induced formation of inositol phosphates in guinea-pig lung.

1. The effects of a novel anti-asthmatic drug, 3-isobutyryl-2-isopropylpyrazolo [1,5-a]pyridine (ibudilast, KC-404) on leukotriene D4 (LTD4)-induced formation of inositol phosphates were studied in slices of guinea-pig lung and hippocampus. 2. In guinea-pig lung, ibudilast inhibited LTD4 (0.01-1 microM)-induced formation of inositol monophosphate (IP1) in a concentration-dependent manner (IC50 = 10 microM) without affecting LTD4 receptor binding. 3. Ibudilast (10 microM) inhibited histamine (0.1-1 mM)-induced formation of IP1 in guinea-pig lung slices but not in hippocampal slices. 4. Inhibition of agonist-induced formation of IP1 by ibudilast was non-competitive. 5. Ibudilast had no effect on either GTP- or calcium-stimulated phosphatidylinositol specific-phospholipase C activity of lung membranes. 6. These results suggest that ibudilast has no direct effect on LTD4 receptors, GTP binding proteins (G proteins) or phospholipase C, but inhibits inositol phosphate formation, possibly by interfering with the coupling between receptors and G proteins.

Animals↗

PubMed1990

Effect of diphenylthiocarbazone (dithizone) on glutamate level in hippocampus preparation in vitro and in vivo.

To assess the functional interaction between Zn2+ and glutamate in hippocampus, diphenylthiocarbazone (dithizone), a Zn2+ chelator, was used to alter the glutamate level in hippocampus in vitro and in vivo. Dithizone at the concentration of 1 microM stimulated high K(+)- and veratrine-induced release of [3H]glutamate both in the presence and absence of Ca2+ from rat hippocampal slices preloaded with [3H]glutamate without affecting the release of [3H]gamma-aminobutyric acid and [3H]acetylcholine. Metal chelators other than dithizone did not evoke the [3H]glutamate release at the concentration of 10 microM. Two weeks after the intrahippocampal injection of 20 micrograms of dithizone, both Zn2+ and glutamate levels of the hippocampus significantly decreased with no change in the levels of other metals, amino acids, monoamines and acetylcholine.

Acetylcholine↗

PubMed1990

Inhibition of [3H]glutamate release by Zn2+ in rat hippocampal slices.

Zn2+ at the concentration of 10 microM inhibited the depolarization-induced [3H]glutamate release from the preloaded rat hippocampal slices both in the presence and absence of Ca2+ without affecting [3H]GABA and [3H]ACh release. Of divalent cations tested, Zn2+ and Fe2+ had an inhibitory effect on the release of glutamate.

Acetylcholine↗