자료유형
발행기관
- 대한생리학회-대한약리학회(53)
- 대한약리학회(21)
- 대한생리학회(17)
- 대한수의학회(8)
- 한국탄소학회(6)
- 대한신경정신의학회(2)
- 물리치료재활과학회(2)
- 공주교육대학교 초등교육연구원(1)
- 동아시아문화학회(1)
- 한국경호경비학회(1)
- 한국복합재료학회(1)
- 한국웰니스학회(1)
- 한국헬스커뮤니케이션학회(1)
간행물
- THE KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY(53)
- 대한약리학잡지(21)
- 대한생리학회지(17)
- CARBON LETTERS(6)
- JOURNAL OF VETERINARY SCIENCE(6)
- PHYSICAL THERAPY REHABILITATION SCIENCE(2)
- 신경정신의학(2)
- KOREAN JOURNAL OF VETERINARY RESEARCH(구 대한수의학회지)(1)
- 교육논총(1)
- 대한수의학회 학술대회발표집(1)
- 동아시아문화와예술(1)
- 복합재료 : 한국복합재료학회지(1)
- 시큐리티연구(1)
- 한국웰니스학회지(1)
- 헬스커뮤니케이션연구(1)
전체 선택해제
총 115건 검색
본문검색 결과만 보기
-
Involvement of ERK1/2 and JNK Pathways in 17β-estradiol Induced Kir6.2 and SK2 Upregulation in Rat Osteoblast-like Cells
Jung-WookKim, Eun-KyoungYang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.4 6 199-206 (8 pages)
In addition, treatment of cells with U0126, a specific inhibitor of extracellular receptor kinases (ERK)1/2, and SP600125, a specific inhibitor of c-jun N-terminal kinase (JNK) blocked the enhancing effects of 17β-E2 on SK2 and Kir6.2 protein expressions. On the other hand, blocking of p38 mitogen-activated protein kinase had no effect. Taken together, these results indicate that 17β-E2 modulates SK2 and Kir6.2 expressions through the estrogen receptor, involving ERK1/2 and JNK activations. -
Lysophosphatidylcholine Attenuates Endothelium-dependent Relaxation Responses through Inhibition of ACh-induced Endothelial [Ca2+]i Increase
Seong-ChunKwon, Yong-HoLee, TaicksangNam, Duck-SunAhn 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.1 5 25-30 (6 pages)
Lysophosphatidylcholine (LPC), which accumulates in atherosclerotic arteries, has been reported to inhibit endothelium-dependent relaxation (EDR) in many different species. However, the underlying mechanism of LPC-induced inhibition of EDR is still uncertain. In the present study, we measured simultaneously both isometric tension and cytosolic free Ca2 ([Ca2]i) in rabbit carotid strips, and examined the effect of LPC on tension and [Ca2]i. In carotid strips with... -
Na+-Ca2+ Exchange Curtails Ca2+ before Its Diffusion to Global Ca2+i in the Rat Ventricular Myocyte
Sung-WanAhnChangMannKo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.2 4 95-102 (8 pages)
In the heart, Na-Ca2 exchange (NCX) is the major Ca2 extrusion mechanism. NCX has been considered as a relaxation mechanism, as it reduces global [Ca2]i raised during activation. However, if NCX locates in the close proximity to the ryanodine receptor, then NCX would curtail Ca2 before its diffusion to global Ca2i. This will result in a global [Ca2]i decrease especially during its ascending phase rather than descending phase. Therefore, NCX would... -
Acetylcholine Induces Hyperpolarization Mediated by Activation of K(Ca) Channels in Cultured Chick Myoblasts
DoyunLee, JaeheeHan, Jae-YongPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.1 6 37-44 (8 pages)
by KCa channels provides driving force for Ca2 influx through the stretch-activated channels into the cells. Here, we showed that acetylcholine (ACh) also hyperpolarized the membrane of cultured chick myoblasts, suggesting that nicotinic acetylcholine receptor (nAChR) may be another pathway for Ca2 influx. Under cell-attatched patch configuration, ACh increased the open probability of KCa channels from 0.007 to 0.055 only when extracellular Ca2 was present. Nicotine, a nAChR... -
Buffering Contribution of Mitochondria to the [Ca2+]i Increase by Ca2+ Influx through Background Nonselective Cation Channels in Rabbit Aortic Endothelial Cells
YoungChulKim, SangJinLee, KiWhanKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.1 5 29-36 (8 pages)
To prove the buffering contribution of mitochondria to the increase of intracellular Ca2+ level ([Ca2+]i) via background nonselective cation channel (background NSCC), we examined whether inhibition of mitochondria by protonophore carbonylcyanide m-chlorophenylhydrazone (CCCP) affects endothelial Ca2+ entry and Ca2+ buffering in freshly isolated rabbit aortic endothelial cells (RAECs). The ratio of fluorescence by fura-2 AM (R340/380) was measured in RAECs. Biological state was checked by... -
Heterogeneity of the SR-dependent Inward Na+-Ca2+ Exchange Current in the Heavily Ca2+-buffered Rat Ventricular Myocytes
Kyung-BongYoon, Sung-WanAhn, ChangMannKo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.2 6 101-110 (10 pages)
Voltage-sensitive release mechanism was pharmacologically dissected from the Ca2-induced Ca2 release in the SR Ca2 release in the rat ventricular myocytes patch-clamped in a whole-cell mode. SR Ca2 release process was monitored by using forward-mode Na-Ca2 exchange after restriction of the interactions between Ca2 from SR and Na-Ca2 exchange within micro-domains with heavy cytosolic Ca2 buffering with 10 mM BAPTA. During... -
Role of Stretch-Activated Channels in Stretch-Induced Changes of Electrical Activity
JaeBoumYoum, Su-HyunJo, ChaeHunLeem, Won-KyungHo, YungE. 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2004, Vol.8 No.1 6 33-41 (9 pages)
We developed a cardiac cell model to explain the phenomenon of mechano-electric feedback (MEF), based on the experimental data with rat atrial myocytes. It incorporated the activity of ion channels, pumps, exchangers, and changes of intracellular ion concentration. Changes in membrane excitability and Ca2 transients could then be calculated. In the model, the major ion channels responsible for the stretch-induced changes in electrical activity were the stretch-activated channels (SACs).... -
Comparison of Vasodilator Effects of Platycodin D and D3 in Rats
Dong-YoonLim, Byeong-CheolKim, Eun-BangLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2003, Vol.7 No.3 5 149-155 (7 pages)
D and D3, which are active components derived from the roots of Platycodon grandiflorum A. DC., on the contractile force of the i3olated rat aorta and blood pressure of the anesthetized rat, and also to elucidate its mechanism of action. Both phenylephrine (an adrenergic α1-receptor agonist) and high potassium (a membrane- depolarizing agent) caused great contractile responses in the isolated aortic strips. Platycodin D at high concentration (24μg/ml) inhibited contractile responses induced by... -
Identification of ATP-sensitive K+ Conductances in Male Rat Major Pelvic Ganglion Neurons
Kyu-SangPark, Seung-KyuCha, Keon-IlLee, JaeYeoulJun, Seong-WooJeong, InDeokKong, JoongWooLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2002, Vol.6 No.5 3 247-254 (8 pages)
Major pelvic ganglia (MPG) neurons are classified into sympathetic and parasympathetic neurons according to the electrophysiological properties; membrane capacitance (Cm), expression of T-type Ca2 channels, and the firing patterns during depolarization. In the present study, function and molecular expression of ATP-sensitive K (KATP) channels was investigated in MPG neurons of male rats. Only in parasympathetic MPG neurons showing phasic firing patterns, hyperpolarizing changes... -
Pulse Exposure to Ethanol Augments Vascular Contractility Through Stress Response
Eun-KyoungYangInKyeomKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2001, Vol.5 No.1 7 47-53 (7 pages)
Drinking excessive alcohol has been recognized as a risk factor for hypertension. However, the mechanism by which alcohol intake causes hypertension still remains elusive. We tested the hypothesis that ethanol itself acts as a stress factor on vasculature and indirectly modulates vascular contractility. After end of exposure to 1, 2.5 and 5% ethanol for 45 min, rat aortic strips were subjected to contractile responses, immunoblot for Hsp70 and the measurement of levels of myosin light chain...
