Selective modulation of the ATP-sensitive K+ channel by nicorandil in guinea-pig cardiac cell membrane

1990 ◽  
Vol 342 (5) ◽  
Author(s):  
M. Takano ◽  
A. Noma
Keyword(s):  
Cell Membrane ◽  
Guinea Pig ◽  
K Channel ◽  
Cardiac Cell ◽  
Selective Modulation

scholarly journals On the mechanism of G protein beta gamma subunit activation of the muscarinic K+ channel in guinea pig atrial cell membrane. Comparison with the ATP-sensitive K+ channel.

1992 ◽  
Vol 99 (6) ◽  
pp. 961-983 ◽  
Author(s):  
H Ito ◽  
R T Tung ◽  
T Sugimoto ◽  
I Kobayashi ◽  
K Takahashi ◽  
...  
Keyword(s):  
Cell Membrane ◽  
Guinea Pig ◽  
G Proteins ◽  
Katp Channel ◽  
K Channel ◽  
Channel Activation ◽  
Gamma Subunit ◽  
Internal Solution ◽  
Gamma S ◽  
Atrial Cell

The mechanism of G protein beta gamma subunit (G beta gamma)-induced activation of the muscarinic K+ channel (KACh) in the guinea pig atrial cell membrane was examined using the inside-out patch clamp technique. G beta gamma and GTP-gamma S-bound alpha subunits (G alpha *'s) of pertussis toxin (PT)-sensitive G proteins were purified from bovine brain. Either in the presence or absence of Mg2+, G beta gamma activated the KACh channel in a concentration-dependent fashion. 10 nM G beta gamma almost fully activated the channel in 132 of 134 patches (98.5%). The G beta gamma-induced maximal channel activity was equivalent to or sometimes larger than the GTP-gamma S-induced one. Half-maximal activation occurred at approximately 6 nM G beta gamma. Detergent (CHAPS) and boiled G beta gamma preparation could not activate the KACh channel. G beta gamma suspended by Lubrol PX instead of CHAPS also activated the channel. Even when G beta gamma was pretreated in Mg(2+)-free EDTA internal solution containing GDP analogues (24-48 h) to inactivate possibly contaminating G i alpha *'s, the G beta gamma activated the channel. Furthermore, G beta gamma preincubated with excessive GDP-bound G o alpha did not activate the channel. These results indicate that G beta gamma itself, but neither the detergent CHAPS nor contaminating G i alpha *, activates the KACh channel. Three different kinds of G i alpha * at 10 pM-10 nM could weakly activate the KACh channel. However, they were effective only in 40 of 124 patches (32.2%) and their maximal channel activation was approximately 20% of that induced by GTP-gamma S or G beta gamma. Thus, G i alpha * activation of the KACh channel may not be significant. On the other hand, G i alpha *'s effectively activated the ATP-sensitive K+ channel (KATP) in the ventricular cell membrane when the KATP channel was maintained phosphorylated by the internal solution containing 100 microM Mg.ATP. G beta gamma inhibited adenosine or mACh receptor-mediated, intracellular GTP-induced activation of the KATP channel. G i alpha *'s also activated the phosphorylated KATP channel in the atrial cell membrane, but did not affect the background KACh channel. G beta gamma subsequently applied to the same patch caused prominent KACh channel activation. The above results may indicate two distinct regulatory systems of cardiac K+ channels by PT-sensitive G proteins: G i alpha activation of the KATP channel and G beta gamma activation of the KACh channel.

scholarly journals Weak Electromagnetic Fields Accelerate Fusion of Myoblasts

2021 ◽  
Vol 22 (9) ◽  
pp. 4407
Author(s):  
Dana Adler ◽  
Zehavit Shapira ◽  
Shimon Weiss ◽  
Asher Shainberg ◽  
Abram Katz
Keyword(s):  
Skeletal Muscle ◽  
Cell Membrane ◽  
Cell Fusion ◽  
Electromagnetic Fields ◽  
Muscle Development ◽  
K Channel ◽  
Gambogic Acid ◽  
Cell Replication ◽  
Myotube Formation ◽  
Primary Myoblast

Weak electromagnetic fields (WEF) alter Ca2+ handling in skeletal muscle myotubes. Owing to the involvement of Ca2+ in muscle development, we investigated whether WEF affects fusion of myoblasts in culture. Rat primary myoblast cultures were exposed to WEF (1.75 µT, 16 Hz) for up to six days. Under control conditions, cell fusion and creatine kinase (CK) activity increased in parallel and peaked at 4–6 days. WEF enhanced the extent of fusion after one and two days (by ~40%) vs. control, but not thereafter. Exposure to WEF also enhanced CK activity after two days (almost four-fold), but not afterwards. Incorporation of 3H-thymidine into DNA was enhanced by one-day exposure to WEF (~40%), indicating increased cell replication. Using the potentiometric fluorescent dye di-8-ANEPPS, we found that exposure of cells to 150 mM KCl resulted in depolarization of the cell membrane. However, prior exposure of cells to WEF for one day followed by addition of KCl resulted in hyperpolarization of the cell membrane. Acute exposure of cells to WEF also resulted in hyperpolarization of the cell membrane. Twenty-four hour incubation of myoblasts with gambogic acid, an inhibitor of the inward rectifying K+ channel 2.1 (Kir2.1), did not affect cell fusion, WEF-mediated acceleration of fusion or hyperpolarization. These data demonstrate that WEF accelerates fusion of myoblasts, resulting in myotube formation. The WEF effect is associated with hyperpolarization but WEF does not appear to mediate its effects on fusion by activating Kir2.1 channels.

scholarly journals Large-conductance voltage- and Ca2+-activated K+ channel regulation by protein kinase C in guinea pig urinary bladder smooth muscle

2014 ◽  
Vol 306 (5) ◽  
pp. C460-C470 ◽  
Author(s):  
Kiril L. Hristov ◽  
Amy C. Smith ◽  
Shankar P. Parajuli ◽  
John Malysz ◽  
Georgi V. Petkov
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Bk Channels ◽  
Bk Channel ◽  
K Channel ◽  
Channel Activity ◽  
Open Probability ◽  
Channel Regulation ◽  
Pkc Activation

Large-conductance voltage- and Ca2+-activated K+ (BK) channels are critical regulators of detrusor smooth muscle (DSM) excitability and contractility. PKC modulates the contraction of DSM and BK channel activity in non-DSM cells; however, the cellular mechanism regulating the PKC-BK channel interaction in DSM remains unknown. We provide a novel mechanistic insight into BK channel regulation by PKC in DSM. We used patch-clamp electrophysiology, live-cell Ca2+ imaging, and functional studies of DSM contractility to elucidate BK channel regulation by PKC at cellular and tissue levels. Voltage-clamp experiments showed that pharmacological activation of PKC with PMA inhibited the spontaneous transient BK currents in native freshly isolated guinea pig DSM cells. Current-clamp recordings revealed that PMA significantly depolarized DSM membrane potential and inhibited the spontaneous transient hyperpolarizations in DSM cells. The PMA inhibitory effects on DSM membrane potential were completely abolished by the selective BK channel inhibitor paxilline. Activation of PKC with PMA did not affect the amplitude of the voltage-step-induced whole cell steady-state BK current or the single BK channel open probability (recorded in cell-attached mode) upon inhibition of all major Ca2+ sources for BK channel activation with thapsigargin, ryanodine, and nifedipine. PKC activation with PMA elevated intracellular Ca2+ levels in DSM cells and increased spontaneous phasic and nerve-evoked contractions of DSM isolated strips. Our results support the concept that PKC activation leads to a reduction of BK channel activity in DSM via a Ca2+-dependent mechanism, thus increasing DSM contractility.

Acetylcholine response in guinea pig outer hair cells. II. Activation of a small conductance Ca2+-activated K+ channel

1996 ◽  
Vol 101 (1-2) ◽  
pp. 149-172 ◽  
Author(s):  
Anastas P. Nenov ◽  
Charles Norris ◽  
Richard P. Bobbin
Keyword(s):  
Guinea Pig ◽  
Hair Cells ◽  
Outer Hair Cells ◽  
K Channel ◽  
Small Conductance

Effect of Inhalation Anesthetics on Cardiac Cell Membrane Potentials

1960 ◽  
Vol 21 (1) ◽  
pp. 100-100
Author(s):  
Evan L. Frederickson ◽  
Joseph V. Levy ◽  
K. Ichiyanagi
Keyword(s):  
Cell Membrane ◽  
Membrane Potentials ◽  
Cardiac Cell ◽  
Inhalation Anesthetics

The stimulant action of acetylcholine and catecholamines on the uterus

1973 ◽  
Vol 265 (867) ◽  
pp. 149-156 ◽  
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Guinea Pig ◽  
Membrane Conductance ◽  
Primary Effect ◽  
Force Of Contraction ◽  
Chloride Permeability ◽  
Duration Of Action ◽  
Spike Discharge ◽  
Calcium Permeability

The α action of catecholamines on oestrogen dominated guinea-pig uterus is stimulant. The cell membrane is depolarized, membrane conductance is increased, spike discharge is accelerated and tension develops. This action resembles that of acetylcholine though catecholamines are less potent, and, in equiactive concentrations, catecholamines have a longer latency and a longer duration of action. Evidence, obtained by modifications of the ionic environment, indicates that the depolarization by acetylcholine is due to an increase in sodium and calcium permeability and that acetylcholine can release calcium from intracellular stores. The depolarization by catecholamines is due to an increase in chloride permeability and, in addition, sodium is required for the ensuing increase of spike discharge. Catecholamines produce an increase in the force of contraction, long outlasting their immediate stimulation. Moreover, their effect on membrane potential and membrane conductance persists in the presence of lanthanum. These results suggest that Ca release from intracellular stores may be the primary effect produced by the α action of catecholamines and that the increase in the cytoplasmic Ca 2+ concentration may cause the changes at the cell membrane.

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