scholarly journals Mechanism for reactivation of the ATP-sensitive K+ channel by MgATP complexes in guinea-pig ventricular myocytes.

1994 ◽  
Vol 479 (1) ◽  
pp. 95-107 ◽  
Author(s):  
T Furukawa ◽  
L Virág ◽  
N Furukawa ◽  
T Sawanobori ◽  
M Hiraoka
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
K Channel

5-hydroxydecanoate inhibits ATP-sensitive K+ channel currents in guinea-pig single ventricular myocytes

1992 ◽  
Vol 220 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Tatsuto Notsu ◽  
Kiyokazu Ohhashi ◽  
Isao Tanaka ◽  
Hiroshi Ishikawa ◽  
Takeshi Niho ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
K Channel ◽  
Single Ventricular Myocytes ◽  
Channel Currents

Permeability of time-dependent K+ channel in guinea pig ventricular myocytes to Cs+, Na+, NH4+, and Rb+

1990 ◽  
Vol 259 (5) ◽  
pp. H1448-H1454 ◽  
Author(s):  
R. W. Hadley ◽  
J. R. Hume
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Outward Current ◽  
Time Dependent ◽  
K Channel ◽  
Delayed Rectifier ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Outward Currents

Currents through time-dependent K+ channels (also referred to as IK or the delayed rectifier) were studied with the whole cell patch-clamp technique in isolated guinea pig ventricular myocytes. IK measurements were restricted to the examination of deactivation tail currents. Substitution of various monovalent cations for external K+ produced shifts of the reversal potential of IK. These shifts were used to calculate permeability ratios relative to K+. The permeability sequence for the IK channels was K+ = Rb+ greater than NH4+ = Cs+ greater than Na+. Time-dependent outward currents were also examined when the myocytes were dialyzed with Cs+ instead of K+. A sizeable time-dependent outward current, quite similar to that seen with K+ dialysis, was demonstrated. This current was primarily carried by intracellular Cs+, as the reversal potential of the current shifted 46 mV per 10-fold change of external Cs+ concentration. The significance of Cs+ permeation through IK channels is discussed with respect to the common use of Cs+ in isolating other currents.

scholarly journals Action of nicorandil on ATP-sensitive K+ channel in guinea-pig ventricular myocytes

1991 ◽  
Vol 103 (3) ◽  
pp. 1641-1648 ◽  
Author(s):  
Keiko Nakayama ◽  
Zheng Fan ◽  
Fumiaki Marumo ◽  
Tohru Sawanobori ◽  
Masayasu Hiraoka
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
K Channel

Acetylcholine-sensitive muscarinic K+ channels in mammalian ventricular myocytes

1994 ◽  
Vol 266 (5) ◽  
pp. H1812-H1821 ◽  
Author(s):  
S. Koumi ◽  
J. A. Wasserstrom
Keyword(s):  
Guinea Pig ◽  
Single Channel ◽  
Ventricular Myocytes ◽  
Inward Rectification ◽  
K Channel ◽  
Channel Activity ◽  
Patch Clamp Technique ◽  
Current Voltage ◽  
S 100 ◽  
Relationship Of

Acetylcholine (ACh) is known to increase K+ conductance in the atrium and in pacemaker tissues in the heart. This effect has not been well defined in mammalian ventricular tissues. We have identified and characterized the ACh-sensitive muscarinic K+ channel [IK(ACh)] activity in isolated human, cat, and guinea pig ventricular myocytes using the patch-clamp technique. Application of ACh increased whole cell membrane current in human ventricular myocytes. Current-voltage relationship of the ACh-induced current in ventricle exhibited inward-rectification whose slope conductance was smaller than that in atrium. In single-channel recording from cell-attached patches, IK(ACh) activity was observed when ACh was included in the solution. The channel exhibited a slope conductance of 43 +/- 2 pS. Open times were distributed according to a single exponential function with mean open lifetime of 1.8 +/- 0.3 ms. The channel had conductance and kinetic characteristics similar to human atrial IK(ACh), which had a slope conductance of 43 +/- 3 pS and mean open lifetime of 1.6 +/- 0.3 ms. However, concentration of ACh at half-maximal stimulation (KD) of the channel in ventricle was greater (KD = 0.13 microM) than that in atrium (KD = 0.03 microM). Adenosine caused activation of the same K+ channel. After formation of an excised inside-out patch, channel activity disappeared. Application of GTP (100 microM) or GTP gamma S (100 microM) to the solution caused reactivation of the channel. When myocytes were preincubated with pertussis toxin (PTX), ACh failed to activate these channels, indicating that the PTX-sensitive G protein, Gi, is essential for activation of IK(ACh). IK(ACh) channel activity was also found in cat and guinea pig ventricular myocytes. We conclude that ACh directly activates the IK(ACh) in mammalian ventricular myocytes via Gi in a fashion almost identical to atrial myocytes.

Activation of the ATP-sensitive K+ channel by decavanadate in guinea-pig ventricular myocytes

1993 ◽  
Vol 233 (2-3) ◽  
pp. 219-226 ◽  
Author(s):  
Hitoshi Nakashima ◽  
Masafumi Kakei ◽  
Hiromitsu Tanaka
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
K Channel
Sign in / Sign up

Export Citation Format

Share Document