Satoru Yanagiba

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Involvement of erythropoietin-induced cytosolic free calcium mobilization in activation of mitogen-activated protein kinase and DNA synthesis in vascular smooth muscle cells

Journal of Hypertension (2001)

Tetsu Akimoto Eiji Kusano C. Ito Satoru Yanagiba Makoto Inoue

Human recombinant erythropoietin (rHuEPO) induces cytosolic free calcium ([Ca2+]i) mobilization, an activation of mitogen-activated protein (MAP) kinase and DNA synthesis in several tissues. We explored the mechanism of rHuEPO-induced [Ca2+]i mobilization and its role in the activation of MAP kinase and DNA synthesis in vascular smooth muscle cells (VSMC).[Ca2+]i concentrations were measured by fura-2. MAP kinase activation was analyzed using an immunocomplex kinase assay and Western blotting. DNA synthesis was measured as an incorporation of 5-bromo-2'-deoxyuridine.Although addition of rHuEPO significantly increased [Ca2+]i, either in the presence or absence of extracellular Ca2+, the peak level and sustained elevation of [Ca2+]i were significantly reduced in the absence of extracellular Ca2+. Pretreatment with genistein completely blocked the elevation of [Ca2+]i in both conditions. Calphostin C and staurosporine did not completely block the elevation of [Ca2+]i. Staurosporine reduced its peak level in a dose-dependent manner, whereas calphostin C reduced its peak level at concentrations over 1 nmol/l in the presence of extracellular Ca2+. Similar results to those with staurosporine were observed with nifedipine. In the absence of extracellular Ca2+, their dose-dependent effects disappeared even though rHuEPO increased [Ca2+]i. rHuEPO activated MAP kinase and DNA synthesis, both of which were significantly suppressed by the chelation of intracellular Ca2+.These findings suggest that rHuEPO increases [Ca2+]i by both Ca2+ influx and Ca2+ release from intracellular stores. Tyrosine phosphorylation is critical in the regulation of [Ca2+]i, but protein kinase C activation is important only in the regulation of Ca2+ influx. Dihydropyridine-sensitive L-type Ca2+ channels seem to be involved in rHuEPO-induced Ca2+ influx. In addition, increase of [Ca2+]i by rHuEPO stimulates MAP kinase activation and DNA synthesis in VSMC.

Calphostin C

Calphostin

Staurosporine

10.1097/00004872-200102000-00005

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Citations (23)

Extracellular Cl⁻modulates shrinkage-induced activation of Na⁺/H⁺exchanger in rat mesangial cells

AJP Cell Physiology (2000)

Yukio Miyata Shigeaki Muto Satoru Yanagiba Yasushi Asano

To examine the effect of hyperosmolality on Na + /H + exchanger (NHE) activity in mesangial cells (MCs), we used a pH-sensitive dye, 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein-AM, to measure intracellular pH (pH i ) in a single MC from rat glomeruli. All the experiments were performed in CO 2 /[Formula: see text]-free HEPES solutions. Exposure of MCs to hyperosmotic HEPES solutions (500 mosmol/kgH 2 O) treated with mannitol caused cell alkalinization. The hyperosmolality-induced cell alkalinization was inhibited by 100 μM ethylisopropylamiloride, a specific NHE inhibitor, and was dependent on extracellular Na + . The hyperosmolality shifted the Na + -dependent acid extrusion rate vs. pH i by 0.15–0.3 pH units in the alkaline direction. Removal of extracellular Cl − by replacement with gluconate completely abolished the rate of cell alkalinization induced by hyperosmolality and inhibited the Na + -dependent acid extrusion rate, whereas, under isosmotic conditions, it caused no effect on Na + -dependent pH i recovery rate or Na + -dependent acid extrusion rate. The Cl − -dependent cell alkalinization rate under hyperosmotic conditions was partially inhibited by pretreatment with 5-nitro-2-(3-phenylpropylamino)benzoic acid, DIDS, and colchicine. We conclude: 1) in MCs, hyperosmolality activates NHE to cause cell alkalinization, 2) the acid extrusion rate via NHE is greater under hyperosmotic conditions than under isosmotic conditions at a wide range of pH i , 3) the NHE activation under hyperosmotic conditions, but not under isosmotic conditions, requires extracellular Cl − , and 4) the Cl − -dependent NHE activation under hyperosmotic conditions partly occurs via Cl − channel and microtubule-dependent processes.

Osmotic concentration

Intracellular pH

DIDS

HEPES

Sodium–hydrogen antiporter

10.1152/ajpcell.2000.278.6.c1218

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Citations (26)

Pharmacokinetics of irinotecan hydrochloride (CPT-11) in a hemodialysis patient

Nihon Toseki Igakkai Zasshi (2003)

Yoshitaka Iwazu Makoto Inoue Satoru Yanagiba Yukio Miyata Masaki Okada

塩酸イリノテカン (CPT-11) は, I型DNAトポイソメラーゼ阻害によりDNA合成を阻害し, 広い抗腫瘍スペクトラムを持つ. 血液透析療法中の患者ではCPT-11を減量し使用した報告は一例あるものの, その薬物動態, 透析性についての報告はない. われわれは, 維持血液透析中の大腸癌肝転移例にCPT-11を単回投与し, その薬物動態, 透析性について検討した.症例は58歳, 男性. インフォームドコンセントを得た後, CPT-11 50mg/m2を透析2時間前より90分かけて点滴静注し, 透析開始直後および0.5, 1, 2, 4, 8, 12, 24時間後にCPT-11およびその代謝物質 (SN-38およびSN-38G) の血漿中濃度を測定した. また, 透析開始0.5時間後のダイアライザー前後および透析液中の濃度も測定した.その結果, CPT-11およびSN-38Gは血液透析により除去された. 活性代謝物質であるSN-38は血液透析により直接的には除去されなかったが, CPT-11やSN-38Gが減少するため透析施行中に濃度低下を認めた.CPT-11は胆汁排泄が約80%, 腎排泄が約20%であり, 腎不全患者では投与量を調節する必要がある. 血液透析患者にCPT-11 60mg/m2 (週1回) は, 副作用をきたさず投与可能であった.

SN-38

10.4009/jsdt.36.1625

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The Inferior Vena Cava Diameter as a Marker of Dry Weight in Chronic Hemodialyzed Patients

Artificial Organs (1995)

Yukio Ando Satoru Yanagiba Yasushi Asano

Abstract. We have previously reported that the diameter of the inferior vena cava (IVC) reflects the amount of body fluid in hemodialyzed (HD) patients. The present study was undertaken to depict the criteria of IVC diameters for determining dry weight (DW) in anuric HD patients. In healthy subjects, the maximal diameters during quiet expiration (IVCe) and the minimal diameters during quiet inspiration (IVCi) were 16.7 ± 3.2 and 5.7 ± 5.4 mm, respectively (mean ± SD). The collapsibility index (CI, 1 – IVCi/IVCe), which inversely correlates with the central venous pressure, was 0.68 ± 0.29. In anuric HD patients, the IVCe/CI values before and after HD were 14.9 ± 3.2/0.68 ± 0.24 and 8.2 ± 2.3/0.94 ± 0.09, respectively. IVCe decreased proportionally to the amount of ultrafiltration. In HD patients with hypervolemic pulmonary edema, the IVCe and CI values were 22.4 ± 2.9 and 0.22 ± 0.11, respectively. We proposed that IVCe/CI after HD is 8 ± 3 mm/0.9 ± 0.1 as the markers of DW in anuric HD patients and that an IVCe value ≥22 mm together with a CI ≤0.22 implies the warning level of body fluid retention.

Expiration

10.1111/j.1525-1594.1995.tb02292.x

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Citations (87)

Carpal tunnel syndrome associated with persistent median artery in a hemodialysis patient.

Nihon Toseki Igakkai Zasshi (2000)

Satoru Yanagiba Yukio Ando N Miyaji Izumi Ikematsu Eiji Kusano

長期血液透析患者に通常のアミロイド沈着のみならず正中動脈遺残が正中神経圧迫に関与していると思われた手根管症候群 (CTS) を経験したので報告する. 症例は38歳男性で, 慢性糸球体腎炎による慢性腎不全のため約14年の血液透析歴を有していた. 透析時あるいは労作時に増強する左手指のしびれ・疼痛を認め, Tinel's signおよびPhalen's sign陽性, 正中神経領域での著明な末梢神経伝導速度 (NCV) の低下を認めることより左側手根管症候群 (CTS) と診断した. 手根管部の超音波検査およびMRアンギオグラフィー検査で一部網目状に分岐して正中神経と並走する正中動脈の遺存を認めた. 神経剥離術の術中所見では手根管の狭窄とともに, 正中神経と並走し複雑に分岐する正中動脈の遺存を認め, この血管による正中神経への一部圧排も疑われた. このため血管損傷に注意して慎重に正中神経を剥離し, 術後は症状の著明な軽減を認めた.正中動脈は通常, 胎児期にのみ存在し, 成人での遺存は比較的稀である. 透析患者のCTSの原因あるいは合併症として本症はさらに稀と思われるが, CTSに対する内視鏡下手根管開放術などではこのような血管奇形を伴う血管損傷による出血の可能性があるため, 術前に超音波あるいはMRアンギオグラフィー等による充分な検索が必要と思われる.

10.4009/jsdt.33.369

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Peritoneal Injury by Methylglyoxal in Peritoneal Dialysis

Peritoneal Dialysis International (2006)

Ichiro Hirahara Eiji Kusano Satoru Yanagiba Yukio Miyata Yukio Ando

Peritonealdialysis (PD) is a common treatment for patients with reduced or absent renal function. Long-term PD leads to peritoneal injury with structural changes and functional decline, such as ultrafiltration loss. At worst, peritoneal injury leads to encapsulating peritoneal sclerosis, a serious complication of PD. Glucose degradation products contained in PD fluids contribute to the bioincompatibility of conventional PD fluids. Methylglyoxal (MGO) is an extremely toxic glucose degradation product. The present study examined the injurious effect of MGO on peritoneum in vivo.Male Sprague-Dawley rats (n = 6) were administered PD fluids (pH 5.0) containing 0, 0.66, 2, 6.6, or 20 mmol/L MGO every day for 21 days. On day 22, peritoneal function was estimated by the peritoneal equilibration test. Drained dialysate was analyzed for type IV collagen-7S, matrix metalloproteinase (MMP), and vascular endothelial growth factor (VEGF). Histological analysis was also performed.In rats receiving PD fluids containing more than 0.66 mmol/L MGO, peritoneal function decreased significantly and levels of type IV collagen-7S and MMP-2 in drained dialysate increased significantly. In the 20-mmol/L MGO-treated rats, loss of body weight, expression of VEGF, thickening of the peritoneum, and formation of abdominal cocoon were induced. MMP-2 and VEGF were produced by infiltrating cells in the peritoneum. Type IV collagen was detected in basement membrane of microvessels.MGO induced not only peritoneal injury but also abdominal cocoon formation in vivo. The decline of peritoneal function may result from reconstitution of microvessel basement membrane or neovascularization.

Peritoneal equilibration test

Peritoneal fluid

Peritoneal cavity

10.1177/089686080602600317

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Citations (63)

Modulation of Endothelin-1-Induced Cytosolic Free Calcium Mobilization and Mitogen-Activated Protein Kinase Activation by Erythropoietin in Vascular Smooth Muscle Cells

Kidney & Blood Pressure Research (2001)

Eiji Kusano Tetsu Akimoto Tetsuo Umino Satoru Yanagiba Makoto Inoue

Background: It has been reported that human recombinant erythropoietin (rHuEPO) modulates the sensitivity of the cardiovascular system to vasoconstrictors. We investigated whether rHuEPO has modulative effects on the endothelin-1 (ET-1)-induced elevation of cytosolic free calcium concentration ([Ca2+]i) and mitogen-activated protein (MAP) kinase activation in vascular smooth muscle cells (VSMC). Methods: [Ca2+]i was measured by fura-2/AM, and MAP kinase activation was analyzed by Western blotting. Results: Exposure of VSMC to rHuEPO prior to stimulation with ET-1 enhanced both basal and ET-1-induced elevation of [Ca2+]i in a dose-dependent manner in the presence of extracellular Ca2+. The synergistic effect was also retained in the absence of extracellular Ca2+ after exposure to rHuEPO. However, the effect was diminished in the presence of extracellular Ca2+ combined with the intracellular Ca2+ release inhibitor TMB-8, PKC inhibitor, or PKC depletion. Exposure to rHuEPO also had a synergistic effect on the activation of MAP kinase induced by ET-1; however, this effect was diminished in the presence of the Ca2+ chelator BAPTA-AM. Conclusion: The results suggest that rHuEPO has synergistic effects on ET-1-induced [Ca2+]i mobilization, particularly on intracellular Ca2+ release, and MAP kinase activation in VSMC.

Fura-2

10.1159/000054227

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Citations (8)

AVP inhibits LPS- and IL-1β-stimulated NO and cGMP via V₁receptor in cultured rat mesangial cells

AJP Renal Physiology (1999)

Tetsuo Umino Eiji Kusano Shigeaki Muto Tetsu Akimoto Satoru Yanagiba

The present study examined how arginine vasopressin (AVP) affects nitric oxide (NO) metabolism in cultured rat glomerular mesangial cells (GMC). GMC were incubated with test agents and nitrite, and intracellular cGMP content, inducible nitric oxide synthase (iNOS) mRNA, and iNOS protein were analyzed by the Griess method, enzyme immunoassay, and Northern and Western blotting, respectively. AVP inhibited lipopolysaccharide (LPS)- and interleukin-1beta (IL-1beta)-induced nitrite production in a dose- and time-dependent manner, with concomitant changes in cGMP content, iNOS mRNA, and iNOS protein. This inhibition by AVP was reversed by V1- but not by oxytocin-receptor antagonist. Inhibition by AVP was also reproduced on LPS and interferon-gamma (IFN-gamma). Protein kinase C (PKC) inhibitors reversed AVP inhibition, whereas PKC activator inhibited nitrite production. Although dexamethasone and pyrrolidinedithiocarbamate (PDTC), inhibitors of nuclear factor-kappaB, inhibited nitrite production, further inhibition by AVP was not observed. AVP did not show further inhibition of nitrite production with actinomycin D, an inhibitor of transcription, or cycloheximide, an inhibitor of protein synthesis. In conclusion, AVP inhibits LPS- and IL-1beta-induced NO production through a V1 receptor. The inhibitory action of AVP involves both the activation of PKC and the transcription of iNOS mRNA in cultured rat GMC.

Mesangial cell

10.1152/ajprenal.1999.276.3.f433

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Citations (51)

Combined treatment with nafamostat mesilate and aspirin prevents heparin-induced thrombocytopenia in a hemodialysis patient

Clinical Nephrology (2003)

Hideaki Takahashi Shigeaki Muto Eiko Nakazawa Satoru Yanagiba Y. Masunaga

We report on the management of a 36-year-old hemodialysis patient with heparin-induced thrombocytopenia (HIT, type II) and clot formation in extracorporeal circulation. Platelet aggregation test and measurement of anti-platelet factor 4/heparin complex antibody by enzyme-linked immunosorbent assay revealed to us that our patient had developed HIT. Instead of heparin, we used nafamostat mesilate (NM) as an anticoagulant during hemodialysis, but could not completely prevent HIT-induced thrombocytopenia or clot formation in the extracorporeal circuit. Combined use of NM and aspirin completely inhibited platelet aggregation, decrease in platelet count and clot formation in the extracorporeal circuit.

Heparin-Induced Thrombocytopenia

Extracorporeal

Extracorporeal circulation

10.5414/cnp59458

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Citations (19)

Announcements

Kidney & Blood Pressure Research (2001)

Sunil Bhandari Malcolm Hunter M. Mályusz Wataru Kähler G. Gronow

10.1159/000054230

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Citations (0)