Activation by adrenaline of a low-conductance G protein-dependent K+ channel in mouse pancreatic B cells

Nature ◽  
1991 ◽  
Vol 349 (6304) ◽  
pp. 77-79 ◽  
Author(s):  
Patrik Rorsman ◽  
Krister Bokvist ◽  
Carina Ämmälä ◽  
Per Arkhammar ◽  
Per-Olof Berggren ◽  
...  
Author(s):  
U. Panten ◽  
C. Heipel ◽  
F. Rosenberger ◽  
K. Scheffer ◽  
B.J. Ziinkler ◽  
...  
Keyword(s):  
B Cells ◽  

1993 ◽  
Vol 422 (5) ◽  
pp. 443-448 ◽  
Author(s):  
Carina �mm�l� ◽  
Krister Bokvist ◽  
Olof Larsson ◽  
Per -Olof Berggren ◽  
Patrik Rorsman
Keyword(s):  
B Cells ◽  

1989 ◽  
Vol 257 (6) ◽  
pp. C1119-C1127 ◽  
Author(s):  
K. D. Gillis ◽  
W. M. Gee ◽  
A. Hammoud ◽  
M. L. McDaniel ◽  
L. C. Falke ◽  
...  

Intracellular ATP (ATPi)-sensitive K+ [K+(ATP)] channels are now a recognized site of action of clinically useful hypoglycemic and hyperglycemic sulfonamides. We have further examined the action of these agents on single K+ channels in rat pancreatic B-cells 1) Tolbutamide and glyburide, two hypoglycemic sulfonylureas which decrease K+(ATP) channel activity in the cell-attached patch, affect the kinetics of K+(ATP) channel in a manner similar to glucose. They shorten the duration of the “burst,” or cluster of open channel events, while lengthening the intervals between bursts. 2) The hyperglycemic vasodilator diazoxide increases mean K+(ATP) channel activity in the cell-attached patch as well as in the inside-out excised patch exposed to ATPi. It appears to lengthen channel bursts and shorten the intervals between them. Two structurally similar diuretics, hydrochlorothiazide and furosemide, which have mild hyperglycemic effects, do not increase K+(ATP) channel activity even at clinically toxic concentrations. 3) Neither the sulfonylureas nor diazoxide directly affect the activity of single delayed rectifier K+ channels or single calcium and voltage-activated K+ channels in normal B-cells.


1997 ◽  
Vol 499 (1) ◽  
pp. 65-76 ◽  
Author(s):  
P Gilon ◽  
J Yakel ◽  
J Gromada ◽  
Y Zhu ◽  
J C Henquin ◽  
...  

Diabetologia ◽  
1989 ◽  
Vol 32 (8) ◽  
Author(s):  
F.M. Ashcroft ◽  
M. Kakei ◽  
J.S. Gibson ◽  
D.W. Gray ◽  
R. Sutton
Keyword(s):  
B Cells ◽  

1994 ◽  
Vol 200 (2) ◽  
pp. 860-866 ◽  
Author(s):  
P. Krippeitdrews ◽  
S. Britsch ◽  
F. Lang ◽  
G. Drews

1986 ◽  
Vol 250 (1) ◽  
pp. C90-C94 ◽  
Author(s):  
L. M. Rosario ◽  
E. Rojas

High-resistance microelectrodes were used to measure membrane potential changes in response to increased extracellular K+ concentration ([K+]o; or a test cation X+ such as Li+, Rb+, Cs+, NH+4) in B cells from mouse islets of Langerhans. In the absence of glucose, a sudden increase in [K+]o (or [X+]o), keeping the sum [Na+]o + [K+]o constant (or [Na+]o + [K+]o + [X+]o), induced a rapid depolarization of the membrane. The membrane potential changes were essentially unchanged in the presence of 20 mM tetraethylammonium (TEA). The Goldman-Hodgkin-Katz equation was fitted to the experimental relationship between membrane potential and [K+]o (or [X+]o), and permeability (P) ratios were estimated. In the absence of TEA, P Na/PK was estimated to be approximately 0.046. In the presence of TEA the following ratios were estimated: P Rb/PK = 0.74, P Cs/PK = 0.62, and P NH4/PK = 0.36. From these ratios the following sequence of permeabilities was obtained, PK greater than P Rb greater than P Cs greater than P NH4 greater than P Na. It is proposed that this sequence reflects the selectivity of the intracellular [Ca2+]-activated K+ channel of the pancreatic B cell.


Endocrinology ◽  
1995 ◽  
Vol 136 (2) ◽  
pp. 464-467 ◽  
Author(s):  
P Krippeit-Drews ◽  
G Zempel ◽  
H P Ammon ◽  
F Lang ◽  
G Drews

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