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Role of Calmodulin in the Generation of Reactive Oxygen Species and Apoptosis Induced by Tamoxifen in HepG2 Human Hepatoma Cells
YongSooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2002, Vol.6 No.4 3 187-192 (6 pages)
Tamoxifen, an antiestrogen, has previously been shown to induce apoptosis in HepG2 human hepatoblastoma cells through activation of the pathways independent of estrogen receptors, i.e., intracellular Ca2 increase and generation of reactive oxygen species (ROS). However, the mechanism of tamoxifen to link increased intracellular Ca2 to ROS generation is currently unknown. Thus, in this study we investigated the possible involvement of calmodulin, a Ca2 activated protein, and... -
Upregulation of Renal Renin-Angiotensin System in Rats with Adriamycin-Induced Nephrosis
SooWanKim, JongUnLee, Sang-WoongHan, JunHoRyu, YoonWhaOh, NamHoKim, KiChulChoi, Ho-JungKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 4 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2002, Vol.6 No.2 10 127-130 (4 pages)
expression of renin, cilazapril decreased the expression of ACE to the control level. Cilazapril further increased the expression of AT1R, while it restored the decreased expression of AT2R. The expression of TGF-β1 was increased by the treatment with adriamycin, which was abolished by cilazapril. An altered expression of local RAS components may be causally related with the development of adriamycin-induced nephrosis, in which AT1R is for and AT2R is against the development of nephrosis. -
Activation of ATP-sensitive Potassium Channels by the Predominant Metabolite of Isoflurane in Rabbit Ventricular Myocytes
JinHan, NariKim, EuiyongKim, SungjuKim, KangheeCho 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 11 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.2 7 165-175 (11 pages)
Background: Recent in vivo experimental evidence suggests that isoflurane-induced cardioprotection may involve KATP channel activation. However, it was demonstrated that isoflurane inhibited KATP channel activities in the inside-out patch mode. To explain this discrepancy, the present investigation tested the hypothesis that a metabolite of isoflurane, trifluoroacetic acid (TFA), contributes to isoflurnae-induced cardioprotection via KATP channel activation during myocardial ischemia and... -
Altered Delayed Rectifier K+ Current of Rabbit Coronary Arterial Myocytes in Isoproterenol-Induced Hypertrophy
NariKim, JinHan, EuiyongKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.1 5 33-40 (8 pages)
The aim of present study was to define the cellular mechanisms underlying changes in delayed rectifier K (KDR) channel function in isoproterenol-induced hypertrophy. It has been proposed that KDR channels play a role in regulation of vascular tone by limiting membrane depolarization in arterial smooth muscle cells. The alterations of the properties of coronary KDR channels have not been studied as a possible mechanism for impaired coronary reserve in cardiac hypertrophy. The present... -
Role of Gap Junctions in the Endothelium-Dependent Hyperpolarization of Vascular Smooth Muscle Cells
YoshimichiYamamoto, MeganF.Klemm, HikaruHashitani, RichardJ.Lang, TsuyoshiSoji, HikaruSuzuki 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.1 1 1-8 (8 pages)
Hyperpolarization of arterial smooth muscle by acetylcholine is considered to be produced by the release of an unidentified chemical substance, an endothelium-derived hyperpolarizing factor (EDHF). Several chemicals have been proposed as the candidate for EDHF. However, none of them fulfil completely the nature and property of EDHF. Ultrastructural observation with electron microscope reveals that in some arteries, gap junctions are formed between endothelial and smooth muscle cells. In small... -
The Effect of Carbon Monoxide on Contraction, Cytosolic Ca2+ Level and Ionic Currents in Guinea Pig Ileal Smooth Muscle
SeongChunKwon, SeungSooChung, YunSukKim, TaickSangNam 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.6 6 471-477 (7 pages)
The aim of this study was to clarify the mechanism of the inhibitory action of carbon monoxide (CO) on contraction, by measuring cytosolic Ca2 level ([Ca2]i) and ionic currents in guinea-pig ileum. CO (10%) inhibited 40 mM KCl-induced contraction and this effect was blocked by ODQ (1μM), a soluble guanylyl cyclase (sGC) inhibitor. CO inhibited the 40 mM KCl-induced contraction without changing [Ca2]i. Cumulative addition of KCl induced a graded increase in [Ca2]i... -
Effect of Propofol, an Intravenous Anesthetic Agent, on KATP Channels of Pancreatic β-cells in Rats
EunJeePark, Dae-KyuSong, JaeKyuCheun, JungInBae, Won-KyungHo, YungEEarm 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2000, Vol.4 No.1 4 25-31 (7 pages)
from the slope of the relationship between single channel current and pipette potential (20∼100 mV) was not significantly altered by propofol (control: 60.0⁑2.7 pS, 0.1 mM propofol: 58.7⁑3.5 pS). However, mean closed time was surely increased. Above results indicate that propofol blocks the KATP channels in the pancreatic beta cells in the range of its blood concentrations during anesthesia, suggesting a possible effect on insulin secretion and blood glucose level. -
Effects of Bradykinin on Intracellular Calcium Transients in Cardiac Myocytes
Choon-OkPark, YangMiKim, JaeHeeHan, DavidG.Allen, SeongGeunHong 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.6 10 615-621 (7 pages)
In spite many evidences has supported the cardioprotective effect of bradykinin, its direct effects at the cell level are still under question. We investigated the both effects of bradykinin (BK) on Ca2-related ionic currents using whole cell voltage clamp technique in rabbit cardiomyocytes and on the intracellular Ca2 transient using calcium sensitive fluorescence dye, indo-1AM. Simultaneously with recording intracellular Ca2 transients, cell contractility was estimated... -
Effect of C1 Esterase Inhibitor on the Cardiac Dysfunction Following Ischemia and Reperfusion in the Isolated Perfused Rat Heart
Geon-YoungLee, Yong-KyooShin, Yoon-YoungJang, Jin-HoSong, Dae-JoongKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.6 6 579-586 (8 pages)
Complement-mediated neutrophil activation has been hypothesized to be an important mechanism of reperfusion injury. It has been proposed that C1 esterase inhibitor (C1 INH) may prevent the complement- dependent activation of polymorphonuclear leukocytes (PMNs) that occurs within postischemic myocardium. Therefore, The effect of C1 INH was examined in neutrophil dependent isolated perfused rat heart model of ischemia (I) (20 min) and reperfusion (R) (45 min). Administration of C1 INH (5 mg/Kg)... -
Hemorrhage- and Restraint-induced Analgesia in Male and Female Conscious Rats
SungYunOh, HeeSeokHan, DongKukAhn, JaeSikPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 1999, Vol.3 No.6 3 555-563 (9 pages)
It is well known that stress induces analgesia. This study was designed to demonstrate the stress-induced analgesia by employing hemorrhage and restraint and to investigate its mechanism and sex difference. The degree of pain was assessed by measuring the magnitude of jaw opening reflex produced by a noxious electrical stimulation in the dental pulp and by measuring the latency to withdraw the tail from a heat ray. Restraint showed an antinociceptive response. A significant increase in pain...


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