Search

Your search keyword '"Isobe, Hirotaka"' showing total 39 results
Start Over Author "Isobe, Hirotaka"
39 results on '"Isobe, Hirotaka"'

3. Regulation of the genes for arginase isoforms and related enzymes in mouse macrophages by lipopolysaccharide

Author

Salimuddin, Nagasaki, Akitoshi, Gotoh, Tomomi, Isobe, Hirotaka, and Mori, Masataka

Subjects
Endotoxins -- Physiological aspects, Arginase -- Physiological aspects, Nitric oxide -- Physiological aspects, Macrophages -- Physiological aspects, Mice -- Physiological aspects, Biological sciences
Abstract

The early induction of inducible nitric oxide synthase (iNOS) and arginase II in the lung and spleen of mice treated with bacterial lipopolysaccharides has been studied. RNA blot and immunoblot analyses as well as enzyme assay were used in examining the expression of arginase isoforms and related enzymes in mouse tissues and in peritoneal macrophages. Results indicate that iNOS and arginase II were induced early in the lung and spleen of mice but arginase I was induced later in the lung. There was also an early induction of iNOS, arginase II, argininosuccinate synthase and ornithine decarboxylase in peritoneal macrophages.

Published
1999

38. Urinary trypsin inhibitor reduces LPS-induced hypotension by suppressing tumor necrosis factor-alpha production through inhibition of Egr-1 expression.

Author

Molor-Erdene P, Okajima K, Isobe H, Uchiba M, Harada N, and Okabe H

Subjects
Animals, Drug Interactions, Humans, Hypotension chemically induced, Hypotension metabolism, In Vitro Techniques, Lung physiology, Male, Mitogen-Activated Protein Kinase 1 metabolism, Mitogen-Activated Protein Kinase 3 metabolism, Monocytes drug effects, Monocytes metabolism, NF-kappa B metabolism, Nitrates blood, Nitric Oxide Synthase genetics, Nitric Oxide Synthase metabolism, Nitric Oxide Synthase Type II, Nitrites blood, Phosphorylation, RNA, Messenger metabolism, Rats, Rats, Wistar, Transcription Factor AP-1 metabolism, Tumor Necrosis Factor-alpha genetics, Glycoproteins pharmacology, Hypotension drug therapy, Insulin-Like Growth Factor I metabolism, Lipopolysaccharides pharmacology, Tumor Necrosis Factor-alpha metabolism
Abstract

Although urinary trypsin inhibitor (UTI) has been shown to inhibit tumor necrosis factor (TNF)-alpha- production, the detailed mechanism(s) remains unclear. This study was undertaken to elucidate the molecular mechanism(s) underlying this inhibitory effect in monocytes in vitro and in rats given lipopolysaccharide (LPS). TNF-alpha production by monocytes stimulated with LPS (100 ng/ml) was inhibited by UTI at concentrations higher than 100 U/ml. Expression of early growth response factor-1 (Egr-1) and phosphorylation of extracellular signal-regulated protein kinases 1/2 in monocytes stimulated with LPS were inhibited by UTI. UTI (50,000 U/kg i.v.) inhibited LPS (5 mg/kg i.v.)-induced increases in lung tissue levels of Egr-1, TNF-alpha mRNA, and TNF-alpha in rats. UTI inhibited LPS-induced hypotension by inhibiting pulmonary induction of inducible nitric oxide synthase (iNOS). We previously demonstrated that anti-TNF-alpha antibody and aminoguanidine, a selective inhibitor of iNOS, reduced LPS-induced hypotension in this animal model. Furthermore, we also reported that reduction of LPS-induced coagulation abnormalities in rats did not affect inflammatory responses and hypotension in this animal model. Taken together, these observations strongly suggested that UTI inhibited LPS-induced production of TNF-alpha by inhibiting activation of the extracellular signal-regulated protein kinases 1/2-Egr-1 pathway in monocytes, which might at least partly contribute to reduction of hypotension through inhibition of iNOS induction in rats given LPS.

Published
2005
Full Text
View/download PDF

39. Activation of capsaicin-sensitive sensory neurons by carvedilol, a nonselective beta-blocker, in spontaneous hypertensive rats.

Author

Okajima K, Harada N, Uchiba M, and Isobe H

Subjects
Adrenergic alpha-Antagonists pharmacology, Animals, Bisoprolol pharmacology, Blood Pressure drug effects, Calcitonin Gene-Related Peptide blood, Capsaicin pharmacology, Carvedilol, Cells, Cultured, Drug Interactions, Female, Humans, Hypertension blood, Kidney drug effects, Kidney physiology, Male, Mice, Prazosin pharmacology, Rats, Rats, Inbred SHR, Rats, Sprague-Dawley, Regional Blood Flow drug effects, Adrenergic beta-Antagonists pharmacology, Capsaicin analogs & derivatives, Carbazoles pharmacology, Neurons, Afferent drug effects, Propanolamines pharmacology
Abstract

We performed a study in spontaneous hypertensive rats (SHR) to determine whether carvedilol, a nonselective beta-adrenoceptor antagonist, activates capsaicin-sensitive sensory neurons (CSSNs), thereby promoting the release of calcitonin gene-related peptide (CGRP), a neuropeptide with an important role in maintenance of cardiovascular homeostasis. Carvedilol given intravenously at a dose of 0.3 mg/kg transiently decreased the mean arterial blood pressure (MABP) and increased renal tissue blood flow with increases in CGRP levels in plasma and kidney. These effects induced by carvedilol were not seen in animals pretreated with capsazepine, an antagonist of capsaicin. Although 1.0 mg/kg cavedilol markedly decreased MABP, it neither increased renal tissue blood flow nor CGRP levels in plasma and kidney. Prazosin, a selective alpha(1)-adrenoceptor antagonist, and bisoprolol, a selective beta(1)-adrenoceptor antagonist, decreased MABP with capsazepine, showing no antagonistic action in either cases, and these agents increased neither renal tissue blood flow nor levels of CGRP in plasma and kidney. Both ICI 118,551 [(+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol], a selective beta(2)-adrenoceptor antagonist, at a dose of 0.25 mg/kg and capsaicin mimicked effects induced by 0.3 mg/kg carvedilol. Administration of 1.0 mg/kg ICI 118,551 produced effects similar to those induced by 1.0 mg/kg carvedilol. These observations strongly suggested that the low dose of carvedilol might activate CSSNs in SHR to increase the release of CGRP, thereby decreasing blood pressure with an increase in renal tissue blood flow. The effects induced by carvedilol seemed to be mediated by its beta(2)-adrenoceptor blockade activity.

Published
2004
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results