Molecular analysis of ATP-sensitive K+ channel subunits expressed in mouse portal vein

2015 ◽  
Vol 75 ◽  
pp. 29-39 ◽  
Author(s):  
Tadashi Yamamoto ◽  
Kohei Takahara ◽  
Tetsuichiro Inai ◽  
Koichi Node ◽  
Noriyoshi Teramoto
2006 ◽  
Vol 33 (S 1) ◽  
Author(s):  
G. Naros ◽  
O. Yalcin ◽  
S. Maljevic ◽  
T.V. Wuttke ◽  
A. Dervent ◽  
...  

1996 ◽  
Vol 78 (6) ◽  
pp. 1105-1114 ◽  
Author(s):  
Sarita W. Yeola ◽  
Tom C. Rich ◽  
Vic N. Uebele ◽  
Michael M. Tamkun ◽  
Dirk J. Snyders

1994 ◽  
Vol 266 (5) ◽  
pp. H1687-H1698 ◽  
Author(s):  
M. Kamouchi ◽  
K. Kitamura

The modulation of ATP-sensitive K+ (KATP)-channel activity was investigated by recording single-channel currents in isolated smooth muscle cells from rabbit portal vein. K(+)-channel openers (KCOs; pinacidil, lemakalim, and nicorandil) induced burstlike openings of single KATP channels in the cell-attached configuration. After patch excision, KATP channels showed "run-down" phenomenon in the presence of KCOs, but subsequent application of Mg-ATP (1 mM) restored KATP-channel activity. Removal of Mg-ATP resulted in transient augmentation of KATP currents, which eventually decayed out. Nucleotide diphosphates (NDPs; GDP, ADP, UDP, IDP, and CDP) also induced channel reopening in the presence of KCOs, which was markedly enhanced by addition of Mg2+ in millimolar concentrations at the internal side of the membrane. The dose-response relation between ATP and the UDP-induced KATP-channel activity was shifted to the right in the presence of Mg2+ (2 mM). These results suggest that intracellular ATP, NDPs, and Mg2+ regulate the channel state of KATP channels (operative and inoperative states) and that KCOs open KATP channels only in the operative state.


1993 ◽  
Vol 347 (3) ◽  
pp. 329-335 ◽  
Author(s):  
Masahiro Kamouchi ◽  
Shunichi Kajioka ◽  
Takeshi Sakai ◽  
Kenji Kitamura ◽  
Hirosi Kuriyama

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