scholarly journals Glibenclamide Specifically Blocks ATP-Sensitive K<+ Channel Current in Atrial Myocytes of Guinea Pig Heart

1990 ◽  
Vol 54 (4) ◽  
pp. 473-477 ◽  
Author(s):  
Eiji HAMADA ◽  
Reiko TAKIKAWA ◽  
Hiroyuki ITO ◽  
Mari IGUCHI ◽  
Akira TERANO ◽  
...  
Keyword(s):  
Guinea Pig ◽  
K Channel ◽  
Atrial Myocytes ◽  
Guinea Pig Heart ◽  
Channel Current

scholarly journals On the mechanism of basal and agonist-induced activation of the G protein-gated muscarinic K+ channel in atrial myocytes of guinea pig heart.

1991 ◽  
Vol 98 (3) ◽  
pp. 517-533 ◽  
Author(s):  
H Ito ◽  
T Sugimoto ◽  
I Kobayashi ◽  
K Takahashi ◽  
T Katada ◽  
...  
Keyword(s):  
Guinea Pig ◽  
G Protein ◽  
K Channel ◽  
Dependent Manner ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Open Probability ◽  
Concentration Dependent Manner ◽  
Guinea Pig Heart ◽  
Gamma S

Using the patch clamp technique, we examined the agonist-free, basal interaction between the muscarinic acetylcholine (m-ACh) receptor and the G protein (GK)-gated muscarinic K+ channel (IK.ACh), and the modification of this interaction by ACh binding to the receptor in single atrial myocytes of guinea pig heart. In the whole cell clamp mode, guanosine-5'-O-(3-thiotriphosphate) (GTP-gamma S) gradually increased the IK.ACh current in the absence of agonists (e.g., acetylcholine). This increase was inhibited in cells that were pretreated with islet-activating protein (IAP, pertussis toxin) or N-ethylmaleimide (NEM). In inside-out patches, even in the absence of agonists, intracellular GTP caused openings of IK.ACh in a concentration-dependent manner in approximately 80% of the patches. Channel activation by GTP in the absence of agonist was much less than that caused by GTP-gamma S. The agonist-independent, GTP-induced activation of IK.ACh was inhibited by the A promoter of IAP (with nicotinamide adenine dinucleotide) or NEM. As the ACh concentration was increased, the GTP-induced maximal open probability of IK.ACh was increased and the GTP concentration for the half-maximal activation of IK.ACh was decreased. Intracellular GDP inhibited the GTP-induced openings of IK.ACh in a concentration-dependent fashion. The half-inhibition of IK.ACh openings occurred at a much lower concentration of GDP in the absence of agonists than in the presence of ACh. From these results, we concluded (a) that the interaction between the m-ACh receptor and GK is essential for basal stimulation of IK.ACh, and (b) that ACh binding to the receptor accelerates the turnover of GK and increases GK's affinity to GTP analogues over GDP.

scholarly journals A Trek-Like K+ Channel Current Inhibited by Norepinephrine in Rat Atrial Myocytes

2014 ◽  
Vol 106 (2) ◽  
pp. 120a
Author(s):  
Richard C. Bond ◽  
Stephanie C. Choisy ◽  
Simon M. Bryant ◽  
Jules C. Hancox ◽  
Andrew F. James
Keyword(s):  
K Channel ◽  
Atrial Myocytes ◽  
Channel Current

Inhibitory effects of class I and IV antiarrhythmic drugs on the Na+-activated K+ channel current in guinea pig ventricular cells

1998 ◽  
Vol 358 (6) ◽  
pp. 641-648 ◽  
Author(s):  
Katsumi Mori ◽  
Satoru Kobayashi ◽  
Toshihiro Saito ◽  
Yoshiaki Masuda ◽  
H. Nakaya
Keyword(s):  
Guinea Pig ◽  
Antiarrhythmic Drugs ◽  
Class I ◽  
K Channel ◽  
Inhibitory Effects ◽  
Channel Current ◽  
Ventricular Cells

Sphingosylphosphocholine is a naturally occurring lipid mediator in blood plasma: a possible role in regulating cardiac function via sphingolipid receptors

2001 ◽  
Vol 355 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Károly LILIOM ◽  
Guoping SUN ◽  
Moritz BÜNEMANN ◽  
Tamás VIRÁG ◽  
Nóra NUSSER ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Blood Plasma ◽  
Threshold Concentration ◽  
K Channel ◽  
Lipid Mediator ◽  
Atrial Myocytes ◽  
Parasympathetic Nerve ◽  
Serum Factors ◽  
Release Of Acetylcholine ◽  
Inwardly Rectifying

Blood plasma and serum contain factors that activate inwardly rectifying GIRK1/GIRK4 K+ channels in atrial myocytes via one or more non-atropine-sensitive receptors coupled to pertussis-toxin-sensitive G-proteins. This channel is also the target of muscarinic M2 receptors activated by the physiological release of acetylcholine from parasympathetic nerve endings. By using a combination of HPLC and TLC techniques with matrix-assisted laser desorption ionization–time-of-flight MS, we purified and identified sphingosine 1-phosphate (SPP) and sphingosylphosphocholine (SPC) as the plasma and serum factors responsible for activating the inwardly rectifying K+ channel (IK). With the use of MS the concentration of SPC was estimated at 50nM in plasma and 130nM in serum; those concentrations exceeded the 1.5nM EC50 measured in guinea-pig atrial myocytes. With the use of reverse-transcriptase-mediated PCR and/or Western blot analysis, we detected Edg1, Edg3, Edg5 and Edg8 as well as OGR1 sphingolipid receptor transcripts and/or proteins. In perfused guinea-pig hearts, SPC exerted a negative chronotropic effect with a threshold concentration of 1µM. SPC was completely removed after perfusion through the coronary circulation at a concentration of 10µM. On the basis of their constitutive presence in plasma, the expression of specific receptors, and a mechanism of ligand inactivation, we propose that SPP and SPC might have a physiologically relevant role in the regulation of the heart.

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