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김영철,Hikaru Suzuki,Wen-Xie Xu,Hikaru Hashitani,최웅,윤효영,박선미,윤세진,이상전,이상진 대한약리학회 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.6
The properties of voltage dependent Ca²+ current (VDCC) were investigated in interstitial cells of Cajal (ICC) distributed in the myenteric layer (ICC-MY) of guinea-pig antrum. In tissue, ICC-MY showed c-Kit positive reactions and produced driving potentials with the amplitude and frequency of about 62 mV and 2 times min-¹, respectively, in the presence of 1μM nifedipine. Single ICC-MY isolated by enzyme treatment also showed c-Kit immunohistochemical reactivity. These cells were also identified by generation of spontaneous inward current under K+-rich pipette solution. The voltage clamp experiments revealed the amplitude of - 329 pA inward current at irregular frequency. With Cs+-rich pipette solution at Vh=−80 mV, ICC-MY produced voltage-dependent inward currents (VDIC), and nifedipine (1μM) blocked VDIC. Therefore, we successfully isolated c-Kit positive single ICC from guinea-pig stomach, and found that ICC-MY potently produced dihydropiridine sensitive L-type voltage-dependent Ca²+ currents (VDCCL).
Young Chul Kim,Hikaru Suzuki,Wen-Xie Xu,Hikaru Hashitani,Woong Choi,Hyo-Yung Yun,Seon-Mee Park,Sei Jin Youn,Sang-Jeon Lee,Sang Jin Lee 대한생리학회-대한약리학회 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.6
The properties of voltage dependent Ca<sup>2+</sup> current (VDCC) were investigated in interstitial cells of Cajal (ICC) distributed in the myenteric layer (ICC-MY) of guinea-pig antrum. In tissue, ICC-MY showed c<i>-Kit</i> positive reactions and produced driving potentials with the amplitude and frequency of about 62 mV and 2 times min<sup>−1</sup>, respectively, in the presence of 1</SUP>ՌM nifedipine. Single ICC-MY isolated by enzyme treatment also showed c<i>-Kit</i> immunohistochemical reactivity. These cells were also identified by generation of spontaneous inward current under K<sup>+</sup>-rich pipette solution. The voltage clamp experiments revealed the amplitude of - 329 pA inward current at irregular frequency. With Cs<sup>+</sup>-rich pipette solution at <i>V</i><sub>h</sub>=−80 mV, ICC-MY produced voltage-dependent inward currents (VDIC), and nifedipine (1ՌM) blocked VDIC. Therefore, we successfully isolated c<i>-Kit</i> positive single ICC from guinea-pig stomach, and found that ICC-MY potently produced dihydropiridine sensitive L-type voltage-dependent Ca<sup>2+</sup> currents (VDCC<sub>L</sub>).
Kim, Young-Chul,Suzuki, Hikaru,Xu, Wen-Xie,Hashitani, Hikaru,Choi, Woong,Yun, Hyo-Yung,Park, Seon-Mee,Youn, Sei-Jin,Lee, Sang-Jeon,Lee, Sang-Jin The Korean Society of Pharmacology 2008 The Korean Journal of Physiology & Pharmacology Vol.12 No.6
The properties of voltage dependent $Ca^{2+}$ current (VDCC) were investigated in interstitial cells of Cajal (ICC) distributed in the myenteric layer (ICC-MY) of guinea-pig antrum. In tissue, ICC-MY showed c-Kit positive reactions and produced driving potentials with the amplitude and frequency of about 62 mV and 2 times $min^{-1}$ respectively, in the presence of $1{\mu}M$ nifedipine. Single ICC-MY isolated by enzyme treatment also showed c-Kit immunohistochemical reactivity. These cells were also identified by generation of spontaneous inward current under $K^+$ -rich pipette solution. The voltage clamp experiments revealed the amplitude of - 329 pA inward current at irregular frequency. With $Cs^+$-rich pipette solution at $V_h=-80\;mV$, ICC-MY produced voltage-dependent inward currents (VDIC), and nifedipine ($1{\mu}M$) blocked VDIC. Therefore, we successfully isolated c-Kit positive single ICC from guinea-pig stomach, and found that ICC-MY potently produced dihydropiridine sensitive L-type voltage-dependent $Ca^{2+}$ currents ($VDCC_L$).
Role of Gap Junctions in the Endothelium-Dependent Hyperpolarization of Vascular Smooth Muscle Cells
Yoshimichi Yamamoto,Megan F. Klemm,Hikaru Hashitani,Richard J. Lang,Tsuyoshi Soji.,Hikaru Suzuki 대한생리학회-대한약리학회 2001 The Korean Journal of Physiology & Pharmacology Vol.5 No.1
<P> 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 arterioles, injection of gap junction permeable dyes into an endothelial cell results in a distribution of the dye to surrounding cells including smooth muscle cells. These observations allow the speculation that myoendothelial gap junctions may have a functional significance. Simultaneous measurement of the electrical responses in both endothelial and smooth muscle cells using the double patch clamp method demonstrates that these two cell types are indeed electrically coupled, indicating that they behave as a functional syncytium. The EDHF-induced hyperpolarization is produced by an activation of Ca<SUP>2</SUP>-sensitive K<SUP></SUP>-channels that are inhibited by charybdotoxin and apamin. Agonists that release EDHF increase [Ca<SUP>2</SUP>]<SUB>i</SUB> in endothelial cells but not in smooth muscle cells. Inhibition of gap junctions with chemical agents abolishes the agonist- induced hyperpolarization in smooth muscle cells but not in endothelial cells. All these observations can be explained if EDHF is an electrotonic signal propagating from endothelium to smooth muscle cells through gap junctions.