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Biomedical subjects

T Muraki

Publications and source records attributed to T Muraki.

At least 55 records · Page 3Linked to original sources
PubMed1997

The differential involvement of von Willebrand factor, fibrinogen and fibronectin in acute experimental thrombosis in rat cerebral and mesenteric microvessels.

Arterial thrombi are primarily composed of platelets. Platelets are bound to injured endothelial cells, sub-endothelial matrices, and other platelets by a range of adhesive proteins. Some of these reactions are governed by shear forces. The role of adhesive proteins in the pathogenesis of arterial thrombosis is not fully understood. The aim of this study was to examine the involvement of von Willebrand factor (vWF), fibrinogen (Fg), and fibronectin (FN) in the formation of microvascular thrombi in vivo using a helium-neon laser-induced thrombosis method. Transmission electron microscopy demonstrated that laser irradiation resulted in platelet-rich thrombosis in arterioles and venules, and revealed that this occurred in the absence of endothelial denudation. The mean wall shear rates in mesenteric arterioles and venules were 641 +/- 40 and 280 +/- 20 s-1, respectively. Shear rates increased approximately fivefold in arterioles and tenfold in venules during the formation of occlusive thrombi. Antibody to vWF inhibited thrombosis in arterioles and venules. Antibodies to Fg and FN inhibited thrombosis in venules but not in arterioles. These results confirm that vWF, Fg and FN were involved in thrombogenesis in vivo and demonstrated that significantly higher shear rates were required for the reactions involving vWF than those involving either Fg or FN.

Adhesiveness↗
PubMed1996

Tolerance to lipopolysaccharide-induced increase in vascular permeability in mouse skin.

We investigated whether tolerance develops to the lipopolysaccharide-induced increase in vascular permeability of mouse skin on pretreatment with Salmonella typhimurium lipopolysaccharide. Lipopolysaccharide-induced plasma extravasation was assessed by determining Pontamine sky blue dye accumulation in the skin where lipopolysaccharide was injected s.c. 2 h previously. When mice were pretreated with lipopolysaccharide (0.15 mg/kg i.p.), the dye leakage induced by s.c. challenge with lipopolysaccharide (400 micrograms/site) was significantly, inhibited for 2-24 h after pretreatment, indicating the development of lipopolysaccharide tolerance. At 4 h after lipopolysaccharide (0.15 mg/kg i.p.), the dose-response curve of dye leakage against the challenge dose of lipopolysaccharide shifted about 2-fold to the higher dose. The dye leakage induced by lipopolysaccharide was inhibited by pretreatment with lipopolysaccharide in a dose-dependent manner (0.05-0.15 mg/kg i.p.). Lipopolysaccharide tolerance was not seen in adrenalectomized mice. When mice were pretreated with lipopolysaccharide and NG-nitro-L-arginine methyl ester (L-NAME), a nitric oxide (NO) synthase inhibitor, at the same time, the hyporesponsiveness to lipopolysaccharide challenge disappeared. However, L-NAME was ineffective to inhibit the development of lipopolysaccharide tolerance when administered 24 h after lipopolysaccharide pretreatment or just before the lipopolysaccharide challenge. Tumor necrosis factor-alpha and interleukin-1 alpha but not interleukin-6 induced a similar hyporesponsiveness to lipopolysaccharide. These results suggest that tolerance develops to the lipopolysaccharide-induced increase in vascular permeability in mouse skin after a single lipopolysaccharide administration and that endogenous glucocorticoids and NO are necessary for induction of lipopolysaccharide tolerance. Hyporesponsiveness induced by lipopolysaccharide pretreatment may be mediated by production of some cytokines such as tumor necrosis factor-alpha or interleukin-1 alpha.

Animals↗
PubMed1996

Role of nitric oxide and prostaglandins in lipopolysaccharide-induced increase in vascular permeability in mouse skin.

To examine the possible role of increased vascular permeability in the circulatory shock induced by endotoxin (lipopolysaccharide), we examined whether lipopolysaccharide elicits plasma extravasation in the skin of ddY strain mice. We also studied whether nitric oxide (NO) and prostaglandins may mediate the lipopolysaccharide-induced increase in vascular permeability. Subcutaneous injection of lipopolysaccharide (100-400 micrograms/site) induced a dose-related and delayed increase in vascular permeability at the injection site as determined by the leakage of pontamine sky blue. Concurrent administration of aminoguanidine (a putative inducible NO synthase inhibitor) (10 mg/kg, i.v.) inhibited the lipopolysaccharide (400 micrograms/site)-induced dye leakage by 71%. N(G)-Nitro-L-arginine methyl ester (an inhibitor for both constitutive and inducible NO synthase) (10 and 20 mg/kg, i.v.) inhibited the lipopolysaccharide-induced dye leakage by 36% and 54%, respectively, whereas the inactive enantiomer, N(G)-nitro-D-arginine methyl ester (10 mg/kg, i.v.), had no effect. Pretreatment with an intraperitoneal injection of dexamethasone (500 micrograms/kg) or indomethacin (a cyclooxygenase-1 and -2 inhibitor) (5 mg/kg) almost completely inhibited the response induced by lipopolysaccharide, by 96% and 84%, respectively. [N-(2-Cyclohexyloxy-4-nitrophenyl) methanesulphonamide (a cyclooxygenase-2-specific inhibitor) (0.01-1 mg/kg, i.p.) also induced a dose-related inhibition of dye leakage elicited by lipopolysaccharide: 38% and 80% suppression at the doses of 0.1 and 1 mg/kg, respectively. Cycloheximide (a protein biosynthesis inhibitor) (35 mg/kg, s.c.) suppressed the effect of lipopolysaccharide by 74%. These results suggest that the increase in vascular permeability induced by lipopolysaccharide is mediated by both NO and prostaglandins and that synthesis of inducible NO synthase and cyclooxygenase-2 may be involved in this effect of lipopolysaccharide.

Animals↗
PubMed1996

Angiotensin converting enzyme inhibitor normalizes vascular natriuretic peptide type A receptor gene expression via bradykinin-dependent mechanism in hypertensive rats.

We previously demonstrated that angiotensin converting enzyme (ACE) inhibitor normalizes the up-regulated gene expression of vascular natriuretic peptide type A (NP-A) receptor in hypertensive rats. To elucidate the mechanism, we examined the effect of angiotensin II receptor (AT1) antagonist (TCV-116) and bradykinin receptor (B2) antagonist (Hoe 140) on the NP-A receptor mRNA level in the aorta of genetically hypertensive rats (SHR-SP/Izm) using ribonuclease protection assay. The effect of ACE inhibitor on the NP-A receptor mRNA level was completely abolished by a concomitant administration of Hoe 140, while TCV-116 did not show any significant effect on the NP-A receptor mRNA level. These results suggest that bradykinin plays an important role in the regulation of the vascular NP-A receptor gene expression.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1996

Histochemical staining of cadmium with 2-(8-quinolylazo)-4,5-diphenylimidazole.

In order to develop a stain with increased sensitivity and selectivity for cadmium (Cd), we synthesized and characterized 2-(8-quinolylazo)-4,5-diphenylimidazole (QAI). This chelating agent was more than twice as sensitive for Cd than the best conventional staining agents, including benzothiazolylazo-beta-naphthol. Differentiation between Cd and zinc (Zn) was achieved by immersing tissue sections in TRIS(2-aminoethyl)amine before they were stained with QAI. This pretreatment made it possible to selectively stain for Cd by blocking Zn.

Animals↗
PubMed1996

Identification and cloning of a novel cDNA belonging to tetratricopeptide repeat gene family from Down syndrome-critical region 21q22.2.

We identified and cloned a novel 9,078-bp cDNA, designated TPRDI, from the Down syndrome-critical region by exon trapping. The cDNA encodes a putative protein (TPRDI) of 2,025 amino acid residues. Two isoforms, TPRDII (8,992 bp) and TPRDIII (7,416 bp), were also isolated. TPRDII, which is probably an alternative splicing product from the TPRD gene transcript, encodes two large open reading frames (ORFs) of 200 amino acid residues and 1,792 amino acid residues, respectively. TPRDIII, which is probably generated by transcription from an alternative start site of the TPRD gene, encodes a putative protein of 1,715 amino acid residues (TPRDIII). Northern blot analysis revealed that TPRDI and its isoforms are present in 7-17 day mouse embryo and in all the human adult and fetal tissues examined. TPRDI has three units of a 34-amino-acid repeat similar to the tetratricopeptide repeat (TPR) motif, which may mediate interaction with various proteins. A larger ORF encoded by TPRDII also has three units of TPR motif, but TPRDIII has only two-thirds of this motif unit. Thus, the TPRD gene may belong to the TPR gene family. Near-central and C terminal regions of TPRDs showed some homology to several matrix proteins such as trichohyalin and bullous pemphigoid antigen. It is possible that the TPRD gene is one of the genes whose overexpression causes several morphological anomalies observed in Down syndrome.

Amino Acid Sequence↗
PubMed1996

Vascular action of circulating and local natriuretic peptide systems is potentiated in obese/hyperglycemic and hypertensive rats.

Hypertension is commonly associated with diabetes mellitus. The aim of the present study was to explore the pathophysiological significance of the natriuretic peptide (NP) system in hypertension associated with genetically obese/hyperglycemic Wistar fatty rats. The messenger RNA (mRNA) levels of the two biologically active NP receptors, NP-A receptor [more specific for atrial natriuretic peptide (ANP)] and NP-B receptor [more specific for C-type natriuretic peptide (CNP)], and CNP mRNA levels were determined in the aorta and kidney by ribonuclease protection assay. Plasma ANP levels were determined by RIA. Both NP-A and NP-B receptor mRNA levels in the aortae of Wistar fatty rats were double those in Wistar lean rats. Plasma ANP levels and CNP mRNA levels in the aorta of Wistar fatty rats were also significantly higher than those in Wistar lean rats. In contrast, there was no significant difference in renal levels of the mRNA for both NP receptors and CNP between the two strains. Administration of a NP-A and -B receptor antagonist, HS-142-1, to Wistar fatty rats resulted in a significant increase in systolic blood pressure and a larger decrease in plasma cGMP level than that in Wistar lean rats, with no difference in the extents of decrease in urine volume and urinary sodium excretion between the two strains. These results suggest that both the ANP/NP-A system and the CNP/NP-B system in vessels are up-regulated at the level of gene expression and may, thus, play an important role in counteracting the hypertension associated with diabetes mellitus.

Animals↗
PubMed1996

Angiotensin II-dependent down-regulation of vascular natriuretic peptide type C receptor gene expression in hypertensive rats.

Biological actions of natriuretic peptide (NP) are determined by the condition of the receptor as well as that of the hormone. Although we previously demonstrated in hypertensive rats the up-regulation of NP-A receptor that mediates various biological actions of NPs, the pathophysiologic significance of NP-C receptor, another subtype thought to be related to clearance of NPs and possibly to biological actions, remains unknown. In the present study, we determined NP-C receptor messenger RNA (mRNA) level in the aortic tissue of stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and in cultured aortic smooth muscle cells by ribonuclease protection assay. The aortic NP-C receptor mRNA level in SHR-SP/Izm was significantly lower than that in the control WKY/Izm. Oral administration of an angiotensin (Ang) II receptor (AT1) antagonist, TCV-116, but not a calcium channel blocker, manidipine, reversed the down-regulated NP-C receptor mRNA in SHR-SP/Izm to the level in WKY/Izm, whereas the latter was more potent in decreasing the blood pressure. In cultured aortic smooth muscle cells, the NP-C receptor was the predominant subtype. Ang II decreased the NP-C receptor mRNA level in a dose-dependent manner, but this effect was reversed by an AT1 antagonist, CV-11974. Neither the NP-A nor NP-B receptor mRNA level was altered by Ang II. These findings indicate that vascular NP-C receptor is down- regulated via Ang-II-mediated mechanism in SHR-SP/Izm. The phenomenon, together with the up-regulation of the NP-A receptor, may play an important role in counteracting hypertension by enhancing the action of NPs.

Angiotensin II↗
PubMed1996

Effect of S-ethylisothiourea, a putative inhibitor of inducible nitric oxide synthase, on mouse skin vascular permeability.

By dye leakage in mouse skin, we evaluated the inhibition of proinflammatory stimuli-induced plasma extravasation by a putative inhibitor of inducible nitric oxide synthase, S-ethylisothiourea. A low dose of S-ethylisothiourea (5 micrograms/kg) mimicked aminoguanidine in inhibiting the plasma extravasation elicited by lipopolysaccharide but not by 5-hydroxytryptamine or platelet-activating factor. A higher dose of S-ethylisothiourea (10 micrograms/kg) inhibited the plasma extravasation induced by 5-hydroxytryptamine slightly; however, it increased the basal dye leakage. Thus, S-ethylisothiourea may be used as a relatively specific inhibitor for inducible nitric oxide synthase in vivo.

Animals↗
PubMed1995

Differential gene expression of vascular natriuretic peptide receptor subtype in artery and vein.

Although the vasorelaxation by natriuretic peptide (NP) is much less potent in the vein than in the artery, mechanism underlying the phenomenon remains unknown. Since NP receptor consists of three subtypes with different functions, we determined the mRNA level of each NP receptor subtype in the artery and vein by ribonuclease protection assay. In the aorta, NP-A receptor related to the biological action of NP was the predominant form. By contrast, NP-C receptor related mainly to the clearance of NP was the predominant form in the inferior vena cava: NP-C mRNA level was about two fold higher than in the aorta, while both NP-A and NP-B receptor mRNA levels were about half of that in the aorta. These results provide the molecular basis for the different biological response to NP in the artery and vein. Differential gene expression of NP receptor subtype could be an important determinant of the biological actions of NP.

Animals↗
PubMed1995

Endothelin-1, but not endothelin-3, suppresses lipoprotein lipase gene expression in brown adipocytes differentiated in culture.

The effect of endothelins on lipoprotein lipase activity and lipoprotein lipase mRNA levels was studied in brown adipocytes differentiated in culture. Lipoprotein lipase activity was determined in two fractions; lipoprotein lipase released by heparin (10 IU/ml, 1 h) into the medium (heparin-releasable fraction) and lipoprotein lipase activity remaining in cells (extractable fraction). Time-course studies showed that endothelin 1 (10(-7) M) progressively decreased both lipoprotein lipase fractions (heparin-releasable, extractable), until nadir at 24 h. Endothelin-1 reduced both lipoprotein lipase activities (heparin-releasable, extractable) in a concentration-dependent manner, whereas endothelin-3 did not produce any significant changes in either of them. Northern blot analysis revealed that endothelin-1 (10(-7)-10(-11) M) caused a concentration-dependent decrease in lipoprotein lipase mRNA obtained from cells on day 9. Furthermore, pretreatment of brown adipocytes with endothelin ETA receptor antagonist FR139317 antagonized the endothelin-1-induced reduction of lipoprotein lipase activity and lipoprotein lipase mRNA. These results suggest that endothelin-1 decreases lipoprotein lipase activity by inhibiting the lipoprotein lipase gene expression in brown adipocytes differentiated in culture, possibly through endothelin ETA receptors on cell membranes. Because of marked reduction of lipoprotein lipase activity and its mRNA as a marker of adipogenic differentiation, endothelin-1 may have an inhibitory role in the differentiation of brown adipocytes.

Adipocytes↗
PubMed1995

Developmental changes in response to endothelins and receptor subtypes of isolated rat duodenum.

The response of isolated duodenum to endothelin-1, -3 and IRL 1620 (Suc-[Glu9,Ala11,15]endothelin-1 (8-21)), a selective endothelin ETB receptor agonist, was studied in both neonatal (1-week-old) and adult rats by recording mechanical activity isotonically. Endothelin-1, -3 and IRL 1620 (1-100 nM) elicited sustained contraction of neonatal duodenum, in a concentration-dependent manner, with a potency order of endothelin-1 = endothelin-3 > IRL 1620. The response to endothelin-1 and -3 (10-1000 nM) of adult duodenum was biphasic, i.e., transient relaxation followed by contraction, with a potency order of endothelin-1 > endothelin-3. The contractile response to endothelin-1 of adult but not neonatal duodenum was significantly antagonized by pretreatment with FR139317 (1 microM), an endothelin ETA receptor antagonist. An endothelin ETB receptor antagonist, RES-701-1 (3 microM), weakly antagonized the IRL 1620-induced contraction of neonatal duodenum. However, RES-701-1 (10 microM) did not affect the response to endothelin-1 of either adult or neonatal duodenum. These results indicate that the duodenal response to endothelins changes from a sustained contraction in neonates to a biphasic response in adults. The contractile response to endothelins of neonatal duodenum is suggested to be mediated through endothelin ETB receptors or possibly RES-701-1-resistant ETB receptor subtypes and contraction of adult duodenum through endothelin ETA receptors. The mechanism of the endothelin-induced response of duodenum was also studied.

Aging↗
PubMed1995

Role of eicosanoids but not nitric oxide in the platelet-activating factor-induced increase in vascular permeability in mouse skin.

We investigated the role of endogenous eicosanoids and nitric oxide (NO) in the platelet-activating factor (PAF)-induced increase in vascular permeability in mouse skin. Subcutaneous injection of PAF (45-180 pmol/site) induced a dose-related increase in vascular permeability at the injection site. The vascular permeability induced by PAF (180 pmol/site) was significantly inhibited by pretreatment with an intraperitoneal injection of 1-O-hexadecyl-2-acetyl-sn-glycero-3-phospho (N,N,N-trimethyl) hexanolamine (PAF receptor antagonist) (5 and 25 mg/kg) and indomethacin (cyclooxygenase inhibitor) (10 mg/kg), whereas it was not affected by concurrent intravenous administration of NO synthase inhibitors NG-nitro-L-arginine methyl ester (10 mg/kg) or methylene blue (100 micrograms/kg) nor by topical injection of NG-nitro-L-arginine methyl ester. The inhibitory effect of indomethacin was partially reversed by topical administration of prostaglandin E2. These results suggest that PAF increases venular permeability by activating PAF receptors and that plasma extravasation is potentiated by the release of prostanoids which cause arteriolar dilatation. However, NO is not involved in the effect of PAF in mouse skin.

Amino Acid Oxidoreductases↗
PubMed1995

Gene expression of vascular natriuretic peptide receptor in the aorta of hypertensive rats.

1. To elucidate the pathophysiologic role of vascular natriuretic peptide (NP) receptor in hypertension, we determined NP-A and NP-B receptor mRNA levels by means of ribonuclease protection assay in aorta of three types of hypertensive rats. 2. The NP-A receptor mRNA level was higher in stroke-prone spontaneously hypertensive rats (SHR-SP/Izm) and deoxycorticosterone acetate-salt hypertensive rats than that in their respective control rats. On the contrary, the NP-A receptor mRNA level was lower in NG-nitro-L-arginine-methyl ester (L-NAME)-induced hypertensive rats compared with that in the control. 3. The NP-B receptor mRNA level did not show any significant change in all three hypertensive rats compared with their respective controls. 4. The present study suggests that high blood pressure is not the major factor regulating the NP receptor gene expression and also that the receptor subtype is independently regulated from each other.

Animals↗
PubMed1995

Modulation of vascular natriuretic peptide receptor gene expression in hypertensive and obese hyperglycemic rats.

Receptors for natriuretic peptide (NP) consist of three subtypes: NP-A, NP-B, and NP-C. Recent studies in cultured aortic cells have suggested a phenotype-related switching of the vascular NP receptor from NP-A to NP-B. To ascertain the biological significance of the phenomenon in vivo, we developed a sensitive and reproducible ribonuclease protection assay and determined each receptor messenger RNA (mRNA) level in the vascular vessels of stroke-prone spontaneously hypertensive rats, deoxycorticosterone acetate-salt hypertensive rats, and genetically hyperglycemic. Wistar fatty rats and in cultured aortic smooth muscle cells. The aortic NP-A receptor mRNA level was significantly up-regulated in both types of hypertensive rats, whereas the NP-B receptor mRNA level did not show any significant change. Both NP-A and NP-B receptor mRNA levels were significantly up-regulated in Wistar fatty rats compared with the control values. There was no significant up-regulation of NP-A receptor mRNA in the inferior vena cava of the stroke-prone spontaneously hypertensive rats. Although the NP-A receptor was always the predominant subtype in rat aortic tissue, NP-B receptor was the predominant subtype in aortic smooth muscle cells in culture. These findings suggest that up-regulation of the NP-A receptor, but not the subtype switching, is the major modulation of receptor gene expression in both hypertensive and diabetic rats.

Animals↗
PubMed1995

Ameliorative effects of tea catechins on active oxygen-related nerve cell injuries.

Active oxygen species are suggested to be concerned with various senile disorders. Tea catechins, (+)catechin (CA), (-)epicatechin (EC) and (-)epigallocatechin gallate, are polyhydroxy-fravan derivatives from tea leaves and have been proposed to possess active oxygen scavenging effect. Tea catechins protected the cultured newborn-mouse cerebral nerve cells from death induced by glucose oxidase. The protective potency of (-)epigallocatechin gallate was weaker than those of EC and CA. Learning ability of mice was assessed by a step-down-type passive avoidance test, and memory impairment of mice was achieved by intracisternal injection of glucose oxidase or cerebral ischemia induced by 10 min occlusion of the common carotid arteries. Intracisternal injection of EC improved the memory impairment induced by intracisternal glucose oxidase, and i.v. injection of CA or EC improved that induced by the cerebral ischemia. CA and EC depressed carrageenin-induced edema in rat hind paw, but (-)epigallocatechin gallate did not. These results suggest that tea catechins ameliorate the injuries or impairments induced by active oxygens through scavenging intracellular active oxygens, and might become useful for protecting human from senile disorders such as dementia.

Animals↗
PubMed1994

Angiotensin converting enzyme inhibitor but not calcium blocker down-regulates gene expression of vascular natriuretic peptide receptor in hypertensive rats.

We have recently found that vascular natriuretic peptide (NP)-A receptor mRNA is upregulated in genetically hypertensive (SHR-SP/Izm) and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. In the present study, we examined the effects of antihypertensive treatments on aortic NP-A receptor mRNA expression in these hypertensive rats using ribonuclease protection assay. Oral administration of an angiotensin converting enzyme inhibitor, derapril, but not a calcium channel blocker, manidipine, produced a significant decrease of the NP-A receptor mRNA level after 4 weeks, while both antihypertensive agents showed similar hypotensive effects. Plasma renin was high in SHR-SP/Izm and low in DOCA-salt rats. These results suggest that the vascular renin-angiotensin system rather than the blood pressure has an important role in the regulation of the vascular NP-A receptor.

Animals↗