scholarly journals Overexpressed A 1 Adenosine Receptors Reduce Activation of Acetylcholine-Sensitive K + Current by Native Muscarinic M 2 Receptors in Rat Atrial Myocytes

2000 ◽  
Vol 86 (6) ◽  
pp. 643-648 ◽  
Author(s):  
Marie-Cécile Wellner-Kienitz ◽  
Kirsten Bender ◽  
Thomas Meyer ◽  
Moritz Bünemann ◽  
Lutz Pott
Keyword(s):  
Adenosine Receptors ◽  
Atrial Myocytes ◽  
K Current

scholarly journals Inhibition of muscarinic K+ current in guinea-pig atrial myocytes by PD 81,723, an allosteric enhancer of adenosine binding to A1 receptors

1997 ◽  
Vol 121 (6) ◽  
pp. 1217-1223 ◽  
Author(s):  
B Brandts ◽  
M Bünemann ◽  
J Hluchy ◽  
G V Sabin ◽  
L Pott
Keyword(s):  
Guinea Pig ◽  
Atrial Myocytes ◽  
K Current

Role of chloride currents in repolarizing rabbit atrial myocytes

1995 ◽  
Vol 268 (5) ◽  
pp. H1992-H2002 ◽  
Author(s):  
Z. Wang ◽  
B. Fermini ◽  
J. Feng ◽  
S. Nattel
Keyword(s):  
Action Potential ◽  
Reversal Potential ◽  
Outward Current ◽  
Cell Voltage ◽  
Disulfonic Acid ◽  
Transient Outward Current ◽  
Atrial Myocytes ◽  
Atrial Cells ◽  
K Current

Rabbit atrial cells manifest a prominent transient outward K+ current (Ito1), but this current recovers slowly from inactivation and is unlikely to be important at physiological rates (3-5 Hz). Depolarization of rabbit atrial cells also elicits a transient Ca(2+)-dependent outward Cl- current (Ito2). To compare the relative magnitude of these transient outward currents at various rates, we applied whole cell voltage-clamp techniques to isolated rabbit atrial myocytes. Whereas peak Ito1 exceeded Ito2 at slow rates (0.1 Hz), Ito1 was strongly reduced as rate was increased (by 97 +/- 2%, mean +/- SE, at 4 Hz), while Ito2 was slightly reduced (by 28 +/- 4%, 4 Hz). The reversal potential of transient outward tail currents at 0.07 Hz was -49 +/- 9 mV, while at 2.5 Hz the reversal potential became -18 +/- 7 mV (calculated Cl- reversal potential -18 mV). The addition of the Cl- transport blocker 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 150 microM) or the replacement of external Cl- with methanesulfonate inhibited a large part of the transient outward current elicited by depolarization at 4 Hz. DIDS and Cl- replacement increased action potential duration in both single rabbit atrial cells and multicellular rabbit atrial preparations. We conclude that the Ca(2+)-dependent Cl- current is substantially larger than the transient K+ current at physiological rates in the rabbit and is likely to play a more important role in action potential repolarization than the latter current in this tissue in vivo.

Delayed rectifier K+ current in rabbit atrial myocytes

1995 ◽  
Vol 269 (2) ◽  
pp. H524-H532 ◽  
Author(s):  
K. Muraki ◽  
Y. Imaizumi ◽  
M. Watanabe ◽  
Y. Habuchi ◽  
W. R. Giles
Keyword(s):  
Maximum Amplitude ◽  
Outward Current ◽  
Cell Voltage ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Delayed Rectifier ◽  
Wave Form ◽  
Class Iii ◽  
Atrial Myocytes ◽  
K Current

The role of delayed rectifier K+ current(s) (IK) in rabbit left atrium was examined by applying the whole cell voltage-clamp technique to isolated single myocytes. Right-triangular waveforms, which mimic the shape of atrial action potentials (APs), and selective blockers were used to compare the contribution of IK with other K+ currents to repolarization of the APs. IK measured at 34 degrees C in atrial myocytes was very small; the maximum peak amplitude of the tail current (IK,tail) at -40 mV was approximately 50 pA. The IK,tail was almost abolished in most cells (approximately 80%) by the application of 1 microM E-4031, a class III antiarrhythmic drug. The E-4031-sensitive current recorded with the triangular command wave-form showed strong inward rectification and had a maximum amplitude of approximately 30 pA at -40 mV. Total outward current elicited by triangular command pulses depended strongly on stimulation frequency. The main frequency-dependent component was a Ca(2+)-independent transient K+ current (I(t)). I(t) elicited by triangular pulses at 1 Hz was substantially reduced by 4-aminopyridine (4-AP) at potentials positive to 0 mV but was not changed significantly by 1 microM E-4031; 100 microM E-4031 reduced I(t) by approximately 30%. The shape of the APs which were recorded from a single rabbit atrial cell strongly depended on the pulse frequency. Application of 1 microM E-4031 increased action potential duration (APD) in > 50% of cells examined but had little effect on the resting membrane potential (RMP). Application of 0.1 mM BaCl2 also lengthened APD and reduced RMP by approximately 20 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

Differential regulation of voltage-activated potassium currents in cultured human atrial myocytes

1996 ◽  
Vol 271 (4) ◽  
pp. H1609-H1619 ◽  
Author(s):  
S. N. Hatem ◽  
A. Benardeau ◽  
C. Rucker-Martin ◽  
J. L. Samuel ◽  
E. Coraboeuf ◽  
...  
Keyword(s):  
Reversal Potential ◽  
Maximal Response ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes ◽  
Kinase C ◽  
High K ◽  
Highly Sensitive ◽  
K Current ◽  
Current Reversal

To examine whether the two components of the voltage-activated outward K+ current, an initially rapidly inactivating component (Ito,1) and a slowly inactivating sustained component (Isus), in human atrial myocytes are distinct currents differentially regulated, we studied their behavior during serum-induced growth of cultured myocytes. Currents were recorded in whole cell patch clamped myocytes. After 1 wk of culture (day 8), membrane capacitance was twice the value in freshly dissociated myocytes (178.7 +/- 23 vs. 83.1 +/- 5.5 pF; P < 0.001). Ito,1 density did not differ from that in freshly dissociated myocytes (at +40 mV: 4.38 +/- 0.8 vs. 3.71 +/- 0.6 pA/pF), whereas that of Isus was markedly increased (at +40 mV: 9.76 +/- 2 vs. 2.21 +/- 0.29 pA/pF; P < 0.001). After inactivation of Ito,1 by a prepulse, sustained depolarization elicited in cultured myocytes an Isus with a density of 10.22 +/- 1.18 pA/pF and an apparent tail current reversal potential of -73.5 +/- 3.2 mV, indicating high K+ selectivity. Isus was highly sensitive to 4-aminopyridine (55.4 +/- 4.4% inhibition in 50 microM) and to D-600 (with a concentration inhibiting 50% of maximal response of 34.2 x 10(-6) M). Addition of 5-10 nM staurosporine at day 3 prevented cell growth and reduced Ito,1 density but not the increase in Isus density, which was inhibited by 10 microM staurosporine. Our results indicate that Ito,1 and Isus are regulated independently during in vitro myocyte growth in human atrial myocytes and that the increase in Isus density is not mediated by a protein kinase C-dependent pathway.

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