Modulation of the inwardly rectifying K+ channel in isolated human atrial myocytes by ?1-adrenergic stimulation

1995 ◽  
Vol 148 (2) ◽  
Author(s):  
R. Sato ◽  
S-i. Koumi
Keyword(s):  
K Channel ◽  
Atrial Myocytes ◽  
Adrenergic Stimulation ◽  
Human Atrial Myocytes ◽  
Inwardly Rectifying

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.

Muscarine-gated K+ channel: subunit stoichiometry and structural domains essential for G protein stimulation

1996 ◽  
Vol 271 (1) ◽  
pp. H379-H385 ◽  
Author(s):  
S. J. Tucker ◽  
M. Pessia ◽  
J. P. Adelman
Keyword(s):  
G Protein ◽  
Xenopus Oocytes ◽  
K Channel ◽  
Channel Activity ◽  
Atrial Myocytes ◽  
Structural Domains ◽  
Maximal Stimulation ◽  
Subunit Stoichiometry ◽  
K Current ◽  
Inwardly Rectifying

Coexpression in Xenopus oocytes of the cloned cardiac inward rectifier subunits Kir 3.1 and Kir 3.4 results in G protein-stimulated channel activity closely resembling the muscarinic channel underlying the inwardly rectifying K+ current in atrial myocytes. To determine the stoichiometry and relative subunit positions within the channel, Kir 3.1 and Kir 3.4 were coexpressed in varying ratios with cloned G beta 1 gamma 2 subunits and also as tandemly linked tetramers with different relative subunit positions. The results reveal that the most efficient channel comprises two subunits of each type in an alternating array within the tetramer. To localize regions important for subunit coassembly and G protein sensitivity, chimeric subunits containing domains from either Kir 3.1, Kir 3.4, or the G protein-insensitive subunit Kir 4.1 were expressed. The results demonstrate that the transmembrane domains dictate the potentiation of the coassembled channels and that, although the NH4- or COOH-termini of both subunits alone can confer G protein sensitivity, both termini are required for maximal stimulation by G beta 1 gamma 2.

Effects of K + channel openers on I K(ATP) of human atrial myocytes at physiological temperatures

2001 ◽  
Vol 363 (2) ◽  
pp. 125-132 ◽  
Author(s):  
Brigitte Pelzmann ◽  
Peter Schaffer ◽  
Eva Bernhart ◽  
Petra Lang ◽  
Heinrich Mächler ◽  
...  
Keyword(s):  
K Channel ◽  
Atrial Myocytes ◽  
Human Atrial Myocytes

Acetylcholine-sensitive potassium channels in human atrial myocytes

1990 ◽  
Vol 259 (6) ◽  
pp. H1730-H1735 ◽  
Author(s):  
R. Sato ◽  
I. Hisatome ◽  
J. A. Wasserstrom ◽  
C. E. Arentzen ◽  
D. H. Singer
Keyword(s):  
Single Channel ◽  
K Channel ◽  
Channel Activity ◽  
Atrial Myocytes ◽  
Open Probability ◽  
Human Atrial Myocytes ◽  
Open Time ◽  
Patch Pipette ◽  
Single Channel Activity ◽  
Gamma S

Single channel recording techniques were used to study acetylcholine (ACh)-sensitive K+ channel activity in human atrial myocytes isolated from specimens obtained during corrective cardiac surgery. Under conditions of cell-attached patch, the presence of ACh in the patch pipette activated K+ channels. Single channel activity occurred in periodic bursts. The channels exhibited a slope conductance of 46 +/- 2 pS inwardly (means +/- SD, n = 4). During a burst, both open and closed time histograms were fitted by a single exponential curve, suggesting the existence of one open and one closed state during a burst. Open probability increased directly with ACh concentration without affecting open time. The channel could be activated by GTP and guanosine 5'-O-(3-thiotriphosphate) (GTP gamma S) (in the presence and absence of ACh in the pipette, respectively). Slope conductance, the response to GTP and GTP gamma S, and the independence of activation from Ca2+ were similar to those for other species. In contrast, sensitivity to ACh appeared diminished compared with frog atrial myocytes.

Developmental differences in L-type calcium current of human atrial myocytes

2004 ◽  
Vol 286 (5) ◽  
pp. H1963-H1969 ◽  
Author(s):  
Srinivas M. Tipparaju ◽  
Rajiv Kumar ◽  
Yanggan Wang ◽  
Ronald W. Joyner ◽  
Mary B. Wagner
Keyword(s):  
Older Adult ◽  
Calcium Current ◽  
Low Dose ◽  
Developmental Differences ◽  
Right Atrial ◽  
Atrial Myocytes ◽  
Adrenergic Stimulation ◽  
Inhibitory Effects ◽  
Human Atrial Myocytes ◽  
Protein Levels

We investigated differences in L-type Ca2+ current ( ICa) between infant (INF, 1–12 mo old), young adult (YAD, 14–18 yr old), and older adult (AD) myocytes from biopsies of right atrial appendages. Basal ICa was smaller in INF myocytes (1.2 ± 0.1 pA/pF, n = 29, 6 ± 1 mo old, 11 patients) than in YAD (2.5 ± 0.2 pA/pF, n = 20, 16 ± 1 yr old, 5 patients) or AD (2.6 ± 0.3 pA/pF, n = 19, 66 ± 3 yr old, 9 patients) myocytes ( P < 0.05). Maximal ICa produced by isoproterenol (Iso) was similar in INF, YAD, and AD cells: 8.4 ± 1.1, 9.6 ± 1.0, and 9.2 ± 1.3 pA/pF, respectively. Efficacy (Emax) was larger in INF (607 ± 50%) than for YAD (371 ± 29%) or AD (455 ± 12%) myocytes. Potency (EC50) was 8- to 10-fold higher in AD (0.82 ± 0.09 nM) or YAD (0.41 ± 0.14 nM) than in INF (7.6 ± 3.5 nM) myocytes. Protein levels were similar for Giα2 but much greater for Giα3 in INF than in AD or YAD atrial tissue. When Giα3 activity was inhibited by inclusion of a Giα3 COOH-terminal decapeptide in the pipette, basal ICa and the response to 10 nM Iso were increased in INF, but not in YAD, cells. We propose that basal ICa and the response to low-dose β-adrenergic stimulation are inhibited in INF (but not YAD or AD) cells as a result of constitutive inhibitory effects of Giα3.

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