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Biomedical subjects

Z Ota

Publications and source records attributed to Z Ota.

At least 235 records · Page 13Linked to original sources
PubMed1985

The effect of nifedipine on CRF-41 and AVP-induced ACTH release in vitro.

The effect of nifedipine on CRF-41- and AVP-induced ACTH release was examined using monolayer cultured rat anterior pituitary cells and pituitary halves. Nifedipine inhibited ACTH release induced by synthetic rat CRF-41 in two systems. In pituitary halves, CRF-41 significantly stimulated both ACTH release and cyclic AMP accumulation. Nifedipine inhibited CRF-41-induced ACTH release and the inhibitory effect of nifedipine on CRF-41-induced ACTH release was accompanied by parallel decrease of cyclic AMP levels in pituitary halves. Nifedipine did not inhibit AVP-induced ACTH release in pituitary halves, and AVP did not significantly affect cyclic AMP accumulation in pituitary halves. These results suggest that CRF-41 stimulates ACTH release through the intracellular cyclic AMP system and calcium-calmodulin system which are accelerated by the influx of extracellular calcium ions. Moreover, it is suggested that the calcium required for AVP-induced ACTH release is derived primarily from intracellular rather than extracellular sources.

Adrenocorticotropic Hormone↗
PubMed1985

Effects of morphine on hypothalamic corticotropin-releasing factor (CRF), norepinephrine and dopamine in non-stressed and stressed rats.

The effects of morphine on the hypothalamic corticotropin-releasing factor (CRF), norepinephrine (NE) and dopamine (DA) concentrations were investigated in non-stressed and stressed rats. Acutely administered morphine stimulated both the synthesis and release of CRF in the hypothalamus, thereby activating the pituitary-adrenocortical system in non-stressed rats, but inhibited the stress-induced CRF synthesis and ACTH-corticosterone secretion. Either a morphine or ether-laparotomy stress reduced NE and DA concentrations in the hypothalamus. A pretreatment with morphine inhibited the stress-induced reduction in the hypothalamic NE and DA concentrations, and induced a significant increase in the DA concentration. These observations suggest that hypothalamic NE and DA are involved in morphine-induced changes in hypothalamo-pituitary-adrenocortical (HPA) activity and that endogenous opiates have a role in regulating CRF secretion by interacting with hypothalamic biogenic amines.

Adrenocorticotropic Hormone↗
PubMed1985

Reticuloendothelial cell function in autoimmune hemolytic anemia (AIHA): studies on the mechanism of peripheral monocyte activation.

We examined the activity of peripheral blood monocytes in patients with autoimmune hemolytic anemia (AIHA) using an in vitro assay of monocyte-macrophage interaction with erythrocytes and an antibody-dependent cell-mediated cytotoxicity (ADCC) assay. The monocytes of AIHA patients in the hemolyzing period phagocytized autologous sensitized red cells and anti-D coated red cells more avidly than normal control monocytes. There was no significant relationship between phagocytic activity and ADCC activity. The activated monocytes phagocytized autologous sensitized red cells, but had no ADCC activity in a short time 51Cr release assay. Phagocytic activity of the patients' monocytes against autologous erythrocytes rapidly decreased after treatment with prednisolone even though the red cell sensitization with antibody remained almost the same as during the hemolyzing period. We postulated that the activation of monocytes in AIHA was due to the "arming" effect of anti-erythrocyte antibody, but we think that other mechanisms may also be involved in the activation of monocytes.

Aged↗
PubMed1985

Stability of rat (human) corticotropin-releasing factor in serum, urine and tissue incubation medium.

The stability of rat (human) CRF in serum, urine and tissue incubation medium was examined using Sephadex gel filtration and CRF radioimmunoassay with anti-rat (human) CRF serum. Human serum after incubation with rat (human) CRF for 1 h at 37 degrees C showed two peaks of CRF immunoreactivity on a Sephadex G-50 fine column. Most of the immunoreactivity coeluted with the rat (human) CRF marker. When rat (human) CRF was incubated with rat liver, kidney or hypothalamus, only 3.1-14.9% of the CRF was recovered at the rat (human) CRF position on gel filtration, and two to four CRF-immunoreactive peaks appeared after the rat (human) CRF marker. When rat (human) CRF was incubated with human urine (pH 6.0) for 24 h at room temperature, one peak of CRF immunoreactivity coeluted with the rat (human) CRF marker on Sephadex gel filtration. The urine extracts of normal rats showed some small peaks of CRF-like immunoreactivity on the Sephadex column, with the main peak appearing after authentic CRF. These results suggest that rat (human) CRF is relatively stable in serum and urine, but is easily degraded by tissue enzymes, with the degraded CRF fragments being excreted in the urine.

Animals↗
PubMed1985

Antibody-dependent cell-mediated cytotoxicity (ADCC) toward human O+ red cells coated with anti-D antibody: comparison between lymphocyte and monocyte ADCC activity.

We investigated the antibody dependent cell-mediated cytotoxicity (ADCC) of lymphocytes and monocytes toward human O+ red cells coated with anti-D antibody using a 51Cr release assay. Lysis of sensitized red cells by lymphocytes occurred rapidly, but monocyte-mediated lysis occurred slowly. This difference might be due to postphagocytic 51Cr release by monocytes. ADCC of lymphocytes increased in proportion to the effector cell number, but large amounts of antibodies were required. In contrast, ADCC of monocytes was independent of the effector/target ratio and very small amounts of antibodies could produce red cell lysis. Large amounts of fluid phase IgG were required to inhibit the lymphocyte ADCC, whereas the monocyte ADCC was markedly inhibited by small amounts of IgG. Monocyte-mediated lysis was completely inhibited by the addition of 10% human AB serum, but lymphocyte-mediated lysis was only slightly inhibited. Purified IgG1 and IgG3 were much more inhibitory to the lysis by both effectors than IgG2 and IgG4 (IgG2 greater than IgG4). Erythrophagocytosis also was inhibited by IgG1 and IgG3. These studies demonstrate that lymphocytes as well as monocytes can cause the lysis of antibody sensitized red cells, and IgG1 and IgG3 subclasses are more important than IgG2 and IgG4 in causing lysis of anti-D coated red cells.

ABO Blood-Group System↗
PubMed1985

Binding differences between nicotine and alpha-bungarotoxin in the rat brain.

Radioreceptor assay (RAA) results in rat brain with 3H-nicotine were compared with those obtained using 125I-alpha-Bungarotoxin (BTX). Scatchard analysis showed that the 3H-nicotine binding site had an average Kd and Bmax of 5.31 nM and 0.047 p moles/mg protein, respectively, and that the corresponding 125I-alpha-BTX binding site values were 0.092 nM and 0.044 p moles/mg protein. Cotinine, which is a nicotine metabolite and has a nicotine-like effect in vivo, inhibited 3H-nicotine binding but did not inhibit 125I-alpha-BTX binding. This result suggests that 3H-nicotine is a more useful ligand than 125I-alpha-BTX for investigating the pharmacological action of nicotine in the brain.

Animals↗
PubMed1985

Specific receptor binding of atrial natriuretic peptide to rat renal cortex.

Radiolabeled receptor assay (RRA) of atrial natriuretic peptide (ANP) was studied in rat kidney membranes. Binding of [125I]-ANP to membrane preparations of rat whole kidney was saturated and show a high affinity (Kd = 0.51 nM). Furthermore, renal cortex membrane had a higher affinity for ANP binding site (Kd = 0.26 nM) than renal medulla membrane (Kd greater than 100 nM). This high affinity ANP receptor site in renal cortex membrane indicated that ANP controlled the balance of water and sodium excretion due to this receptor site in the kidney.

Animals↗
PubMed1985

Reduction of specific arginine-vasopressin binding sites of renal medulla membranes in lithium treated rats.

To elucidate the early effects of lithium treatment on the kidney, arginine-vasopressin (AVP) binding sites in the renal medulla were measured by radiolabeled receptor assay (RRA) in rats injected intraperitoneally with lithium chloride (4 mmol/kg body weight) for 7 days. After the 8th day, urine volume of rats injected lithium (Li group) increased and was significantly larger than that of the control rats that were injected physiological saline (control group). On the same day, the AVP binding capacities of renal medulla membranes of the Li group (Bmax = 28.9 +/- 7.2 fmol/100 micrograms protein) were significantly lower than that of the control group (Bmax = 50.0 +/- 6.3 fmol/100 micrograms protein), but there was no difference in the dissociation constant between the two groups. Our findings suggested that lithium-induced diabetes insipidus was due to a reduction in the number of AVP binding sites in the kidney.

Animals↗
PubMed1984

An endogenous inhibitor of GABA receptor binding.

An endogenous inhibitor of GABA receptor binding was prepared from synaptic membrane of rat brain with 0.05% Triton X-100. The endogenous inhibitor was competitive with GABA for GABA binding sites. The inhibition of GABA receptor binding by the endogenous inhibitor was blocked by the allosteric effect of diazepam. In the presence of diazepam, specific [3H]GABA binding was greater in a medium containing the endogenous inhibitor than in one containing an equal inhibitory potency of GABA, whereas there was no difference in the absence of diazepam. This indicated that the endogenous inhibitor was not GABA itself.

Animals↗
PubMed1984

Effects of transition metals on TRH-receptor interaction.

The interaction of TRH receptors and metal ions was investigated. Although the addition of a physiological serum concentration (20 microM) of Zn2+ or Cu2+ to the TRH radioreceptor assay reaction mixture significantly increased the binding capacity, pretreatment of crude synaptic membranes with Ni2+, Zn2+, Cu2+ or Pd2+ resulted in a significant loss of binding activity. The receptor preparation was bound to [3H]TRH in the presence of 10 mM Ni2+ and was solubilized by Triton X-100. Gel filtration was carried out with cold Tris-HCl-Triton buffer without Ni2+. The molecular weight of the solubilized TRH-macromolecular complex was about 300,000 daltons, and Ni2+ was found in the same fraction as the solubilized TRH-receptor. These results suggest that metal ions have inverse effects in different steps of TRH-receptor interaction and that a TRH-receptor molecule indicates a Ni-binding molecule.

Animals↗
PubMed1984

Interaction of synthetic ovine corticotropin releasing factor and arginine vasopressin on in vitro ACTH release by the anterior pituitary of rats.

Synthetic ovine corticotropin releasing factor (CRF) at 0.03-30 ng/ml evoked a significant linear release of ACTH in pituitary monolayer cell cultures. Arginine vasopressin (AVP) at 3-30 ng/ml induced a slight ACTH release in the same culture system. CRF at 100 ng/ml greatly increased the medium ACTH with intracellular ACTH remaining relatively constant. In perifused pituitary quarters, both AVP and CRF evoked significant release of ACTH. When AVP was added in combination with synthetic ovine CRF, an additive or synergistic effect was observed on the CRF-induced ACTH release in both in vitro systems. Preincubation of cultured pituitary cells with synthetic ovine CRF for 1 h did not have a significant effect on the subsequent AVP-induced ACTH release. However, when cells were preincubated for 6 h with CRF at 1 and 100 ng/ml, the AVP-induced ACTH release was significantly increased, but preincubation with AVP suppressed both the basal and AVP-induced ACTH release. These results suggest that synthetic ovine CRF stimulates not only the release of ACTH but also the synthesis of ACTH and that AVP can evoke significant ACTH release from corticotrophs which have enough releasable ACTH or substances needed for ACTH release under the influence of CRF.

Adrenocorticotropic Hormone↗
PubMed1984

Corticotropin releasing factor (CRF)-like immunoreactivity in the hypothalamus and posterior pituitary of the goat, bovine, rat, monkey and human.

Goat hypothalamic extract prepared by HCl extraction and chromatographed on a Sephadex G-50 column showed two immunoreactive CRF peaks. Most of the immunoreactivity coeluted with synthetic ovine CRF, and a small peak eluted near the void volume. Bovine, monkey, rat and human hypothalamic extracts prepared by acid-acetone or acid-methanol extraction showed three immunoreactive peaks. Most of the immunoreactivity coeluted with ovine CRF, and other smaller peaks eluted near the void volume and slightly before arginine vasopressin. Goat hypothalamic extract showed the highest cross-reactivity with anti-ovine CRF serum, followed by bovine hypothalamic extract. Less cross-reactivity was found in human, rat and monkey hypothalamic extracts. CRF immunoreactivity in goat hypothalamic extract coeluted with ovine CRF on reversed phase high performance liquid chromatography (HPLC) and main CRF immunoreactivity in human and rat hypothalamic extracts eluted slightly later than ovine CRF. These results suggest that there is a heterogeneity among the CRF molecules in these species and that goat CRF may be more similar to that of sheep CRF and the amino acid sequence or molecular weight of other animals CRF may be different from that of sheep CRF. The monkey posterior pituitary and rat neurointermediate lobe showed similar elution patterns of CRF immunoreactivity to their hypothalamic extracts on Sephadex gel filtration and HPLC. These results indicate that the posterior pituitary contains a similar CRF to hypothalamic CRF.

Animals↗
PubMed1984

Effect of angiotensin II, catecholamines and glucocorticoid on corticotropin releasing factor (CRF)-induced ACTH release in pituitary cell cultures.

The effects of angiotensin II, catecholamines and glucocorticoid on CRF-induced ACTH release were examined using rat anterior pituitary cells in monolayer culture. Synthetic ovine CRF induced a significant ACTH release in this system. Angiotensin II produced an additive effect on CRF-induced ACTH release. The ACTH releasing activity of CRF was potentiated by epinephrine and norepinephrine. Dopamine itself at 0.03-30 ng/ml did not show any significant effect on ACTH release, but it inhibited CRF-induced ACTH release. Corticosterone at 10(-7) and 10(-6)M inhibited CRF-induced ACTH release. These results indicate that angiotensin II, catecholamines and glucocorticoid modulate ACTH release at the pituitary level.

Adrenocorticotropic Hormone↗
PubMed1984

Production of monoclonal antibodies to human glomerular basement membrane.

Using the technique of somatic cell fusion, we produced monoclonal antibodies to collagenase-digested human glomerular basement membrane (GBM). Fourteen monoclonal antibodies which reacted with normal human kidney in indirect immunofluorescence (IIF) studies were produced. An analysis of the binding patterns indicated that the antigens recognized could be divided into six broad groups. Monoclonal antibody B3-H10 (Group 1) reacted with only GBM in a fine granular pattern. A5-B12 and B5-C2 (Group 2) reacted with GBM and peritubular capillary in a linear pattern. B2-A12 (Group 3) reacted with only epithelial cells. Al-C9 and A4-E2 (Group 4) showed a mesangial pattern in glomerulus and a lineal pattern in tubular basement membrane (TBM), Bowman's capsule and peritubular capillary. A1-E1, A1-E11, A2-E6, A3-B6, A4-F8 and B5-H2 (Group 5) recognized determinants common to GBM, TBM, Bowman's capsule and/or peritubular capillary. A3-F1 and B5-E10 (Group 6) reacted with TBM and Bowman's capsule. The staining pattern of B3-H10 (Group 1) was characteristic because it was not linear, but finely granular along the GBM. The staining pattern of B2-A12 (Group 3) was also characteristic because only epithelial cells were stained, and processes of epithelial cells were observed as fine fibrils. To the best of our knowledge, these two types of monoclonal antibodies have not been reported previously.

Animals↗