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총 125건 검색
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Nitric Oxide Synthase Mediates Carbon Monoxide-Induced Stimulation of L-type Calcium Currents in Human Jejunal Smooth Muscle Cells
InjaLim, JihyunYun, SeungtaeKim, SoonchulMyung, TaehoKim, HyoweonBang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.3 7 161-166 (6 pages)
L-type Ca2 current was partially blocked by N-(3-(Amino-methyl) benzyl) acetamidine·2HCl (1400W, an iNOS inhibitor). On the other hand, 3-bromo-7-nitroindazole (BNI, a nNOS inhibitor) or N5-(1-Iminoethyl)-L-ornithine dihydrochloride (L-NIO, an eNOS inhibitor) completely blocked the CO effect. These data suggest that low dose of exogenous CO may stimulate all NOS isoforms to increase L-type Ca2 channel through nitric oxide (NO) pathway in human jejunal circular smooth muscle cells. -
Postischemic Treatment with Aminoguanidine Inhibits Peroxynitrite Production in the Peroxynitrite Production in the Rat Hippocampus Following Transient Forebrain Ischemia
Yun-SikChoi, Yeo-HongYoon, JuEunLee, Kyung-OkCho, SeongYunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.1 1 1-5 (5 pages)
Transient forebrain ischemia results in the delayed neuronal death in the CA1 area of the hippocampus. The present study was performed to determine effects of aminoguanidine, a selective iNOS inhibitor, on the generation of peroxynitrite and delayed neuronal death occurring in the hippocampus following transient forebrain ischemia. Transient forebrain ischemia was produced in the conscious rats by four-vessel occlusion for 10 min. Treatment with aminoguanidine (100 mg/kg or 200 mg/kg, i.p.) or... -
The Effect of Carbon Monoxide on L-type Calcium Channel Currents in Human Intestinal Smooth Muscle Cells
InjaLim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.6 10 357-362 (6 pages)
Carbon monoxide (CO) is low molecular weight oxide gas that is endogenously produced under physiological conditions and interacts with another gas, nitric oxide (NO), to act as a gastrointestinal messenger. The aim of this study was to determine the effects of exogenous CO on L-type calcium channel currents of human jejunal circular smooth muscle cells. Cells were voltage clamped with 10 mM barium (Ba2) as the charge carrier, and CO was directly applied into the bath to avoid perfusion... -
Curcumin Attenuates Glial Cell Activation But Cannot Suppress Hippocampal CA3 Neuronal Cell Death in i.c.v. Kanic Acid Injection Model
JaeyoungCho, Pil-JaeKong, WanjooChun, Yeo-OkMoon, Yee-TaePark, So-YoungLim, Sung-SooKim, 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 4 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.6 3 307-310 (4 pages)
Kainic acid (KA) is a structural analogue of glutamate that interacts with specific presynaptic and postsynaptic receptors to potentiate the release and excitatory actions of glutamate. Systemic or intracerebroventricular (i.c.v.) administration of KA to experimental animals elicits multifocal seizures with a predominantly limbic localization, and results in neuronal death of cornu ammonia 1 (CA1), reactive gliosis and biochemical changes in the hippocampus and other limbic structures. Several... -
Inhibitory Effect of Esculetin on the Inducuble Nitric Oxide Synthase Expression in TNF-stimulated 3T3-L1 Adipocytes
Jeong-YehYang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.5 7 283-287 (5 pages)
While nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) is beneficial for host survival, it is also detrimental to the host. Thus, regulation of iNOS gene expression may be an effective therapeutic strategy for the prevention of unwanted reactions at various pathologic conditions. During the screening process for the possible iNOS regulators, we observed that esculetin is a potent inhibitor of cytokine-induced iNOS expression. The treatment of 3T3-L1 adipocytes with the tumor... -
Lipopolysaccharide Inhibits Proliferation of the Cultured Vascular Smooth Muscle Cells by Stimulating Inducible Nitric Oxide Synthase and Subsequent Activation of Guanylate Cyclase
HyoungChulChoi, SangGonLee, JongHoKim, JooYoungKim, UyDongSohn, JeoungHeeHa, KwangYounLee, WonJoonKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.4 7 343-351 (9 pages)
This study was undertaken to investigate the mechanism of lipopolysaccharide (LPS) and nitric oxide (NO) as a regulator of vascular smooth muscle cell (VSMC) proliferation. VSMC was primarily cultured from rat aorta and confirmed by the immunocytochemistry with anti-smooth muscle myosin antibody. The number of viable VSMCs were counted, and lactate dehydrogenase (LDH) activity was measured to assess the degree of cell death. Concentrations of nitrite in the culture medium were measured as an... -
G Protein-Coupled Receptor Signaling in Gastrointestinal Smooth Muscle
UyDongSohn, DongSeokKim, KarnamSMurthy 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 11 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.4 1 287-297 (11 pages)
Contraction of smooth muscle is initiated by an increase in cytosolic Ca2 leading to activation of Ca2/ calmodulin-dependnet myosin light chain (MLC) kinase and phosphorylation of MLC. The types of contraction and signaling mechanisms mediating contraction differ depending on the region. The involvement of these different mechanisms varies depending on the source of Ca2 and the kinetic of Ca2 mobilization. Ca2 mobilizing agonists stimulate different... -
Modulation of Ca2+-Activated Potassium Channels by cGMP- Dependent Signal Transduction Mechanism in Cerebral Arterial Smooth Muscle Cells of the Rabbit
JinHan, NariKim, KwangbokLee, EuiyongKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.6 2 439-444 (6 pages)
The present investigation tested the hypothesis that the activation of protein kinase G (PKG) leads to a phosphorylation of Ca2-activated potassium channel (KCa channel) and is involved in the activation of KCa channel activity in cerebral arterial smooth muscle cells of the rabbit. Single-channel currents were recorded in cell-attached and inside-out patch configurations of patch-clamp techniques. Both molsidomine derivative 3-morpholinosydnonimine-N-ethylcarbamide (SIN-1, 50μM) and... -
Impaired Endothelium-Dependent Relaxation is Mediated by Reduced Production of Nitric Oxide in the Streptozotocin-Induced Diabetic Rats
KyoungSookPark, CukSeongKim, SangWonKang, JinBongPark, Kwang-JinKim, SeokJongChang, ByeongHwaJeon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.3 11 263-270 (8 pages)
in diabetic rats were significantly lower than in non-diabetic rats. Western blot analysis using a monoclonal antibody against endothelial cell nitric oxide synthase (eNOS) revealed that the protein level was lower in the aorta of diabetic rats than in non-diabetic rats. These data indicate that nitric oxide formation and eNOS expression is reduced in diabetes, and this would, in part, account for the impaired endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic rats. -
Differential Effects of Nitric Oxide Synthase Inhibitors in Rats
Jun-HeeLee, ChangYellShin, BongSuKang, JiHoonJeong, KyeongBumChoi, YoungSilMin, JinHakKim, InHoiHuh, UyDongSohn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.2 3 99-104 (6 pages)
We investigated the action of NOS inhibitors on NOS in rats. Both of nitric oxide synthase inhibitors, NG-monomethyl-L-arginine (L-NMMA, 3μM) or NG-nitro-L-arginine methylester (L-NAME, 30μM), augmented phenylephrine (PE, 107 M)-induced contraction which was inhibited by acetylcholine (ACh) in rat thoracic aorta. This augmentation by L-NAME or L-NMMA was attenuated with the treatment of NO precursor, arginine. ACh, however, decreased the augmentation induced by L-NMMA, but not by...
