Activation of ?1-adrenoceptors modulates the inwardly rectifying potassium currents of mammalian atrial myocytes

1992 ◽  
Vol 421 (5) ◽  
pp. 431-439 ◽  
Author(s):  
A. P. Braun ◽  
D. Fedida ◽  
W. R. Giles
2007 ◽  
Vol 292 (1) ◽  
pp. R388-R395 ◽  
Author(s):  
Cristina E. Molina ◽  
Hans Gesser ◽  
Anna Llach ◽  
Lluis Tort ◽  
Leif Hove-Madsen

Application of the current-clamp technique in rainbow trout atrial myocytes has yielded resting membrane potentials that are incompatible with normal atrial function. To investigate this paradox, we recorded the whole membrane current ( Im) and compared membrane potentials recorded in isolated cardiac myocytes and multicellular preparations. Atrial tissue and ventricular myocytes had stable resting potentials of −87 ± 2 mV and −83.9 ± 0.4 mV, respectively. In contrast, 50 out of 59 atrial myocytes had unstable depolarized membrane potentials that were sensitive to the holding current. We hypothesized that this is at least partly due to a small slope conductance of Im around the resting membrane potential in atrial myocytes. In accordance with this hypothesis, the slope conductance of Im was about sevenfold smaller in atrial than in ventricular myocytes. Interestingly, ACh increased Im at −120 mV from 4.3 pA/pF to 27 pA/pF with an EC50 of 45 nM in atrial myocytes. Moreover, 3 nM ACh increased the slope conductance of Im fourfold, shifted its reversal potential from −78 ± 3 to −84 ± 3 mV, and stabilized the resting membrane potential at −92 ± 4 mV. ACh also shortened the action potential in both atrial myocytes and tissue, and this effect was antagonized by atropine. When applied alone, atropine prolonged the action potential in atrial tissue but had no effect on membrane potential, action potential, or Im in isolated atrial myocytes. This suggests that ACh-mediated activation of an inwardly rectifying K+ current can modulate the membrane potential in the trout atrial myocytes and stabilize the resting membrane potential.


2001 ◽  
Vol 355 (1) ◽  
pp. 189-197 ◽  
Author(s):  
Károly LILIOM ◽  
Guoping SUN ◽  
Moritz BÜNEMANN ◽  
Tamás VIRÁG ◽  
Nóra NUSSER ◽  
...  

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.


Life Sciences ◽  
2007 ◽  
Vol 80 (7) ◽  
pp. 665-671 ◽  
Author(s):  
Chunyu Deng ◽  
Xiyong Yu ◽  
Sujuan Kuang ◽  
Wenchang Zhang ◽  
Zhiling Zhou ◽  
...  

2002 ◽  
Vol 39 ◽  
pp. 225
Author(s):  
Fuhua Chen ◽  
Fardard Esmailian ◽  
Wei Sun ◽  
Glenn T. Wetzel ◽  
Jonnalagedda S. Sarma ◽  
...  

1996 ◽  
Vol 271 (4) ◽  
pp. C1221-C1232 ◽  
Author(s):  
X. D. Sun ◽  
M. S. Herness

Inwardly rectifying potassium currents were recorded from taste receptor cells dissociated from the rat tongue with the use of patch-clamp techniques in the whole cell configuration. These currents displayed strong inward rectification at potentials negative to the potassium reversal potential and little outward current at potentials positive to it. With elevations of external potassium concentration, the slope and chord conductance increased, activation shifted toward more depolarized potentials, and the reversal potential varied in a predicted Nernst relationship. These currents were insensitive to 4-aminopyridine and partially blocked by tetraethylammonium. Both barium and cesium gave more complete blocks with characteristic relief at more negative potentials. Inhibition with barium was more voltage sensitive than with cesium. These currents were unaffected by changes in external sodium. The high conductance at negative membrane potentials suggests these currents may contribute with other conductances to the resting potential of taste cells. They may also participate in yet unidentified processes of taste transduction, resulting in the early depolarization of the resting potential.


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