scholarly journals Anti-cholinergic effects of SUN 1165, flecainide, quinidine and disopyramide in isolated atrial myocytes from guinea-pig.

1991 ◽  
Vol 55 ◽  
pp. 178
Author(s):  
Norio Inomata ◽  
Takafumi Ishihara
1997 ◽  
Vol 121 (6) ◽  
pp. 1217-1223 ◽  
Author(s):  
B Brandts ◽  
M Bünemann ◽  
J Hluchy ◽  
G V Sabin ◽  
L Pott
Keyword(s):  

1995 ◽  
Vol 269 (3) ◽  
pp. H1165-H1170 ◽  
Author(s):  
J. R. Berlin

Spatial and temporal changes of intracellular calcium ion concentration ([Ca2+]i) during stimulated contractions were observed by confocal microscopy in rat ventricular and guinea pig atrial myocytes. Fluorescence intensity profiles in fluo 3-acetoxymethyl ester (fluo 3-AM)-loaded cells were collected from the entire cell, selected regions of the cell, or along a single scanned line across the cell. In rat ventricular myocytes, the increase of [Ca2+]i after a single stimulus from field electrodes occurred synchronously across the cell whether fluo 3 fluorescence was monitored in a narrow region aligned with the long axis of the cell or in line-scan images of a single z-line across the cell. However, during the onset of Ca2+ channel blockade by nifedipine (5 microM), electrical stimulation produced spatially nonuniform, focal increases of [Ca2+]i. In guinea pig atrial myocytes, stimulated increases of [Ca2+]i first appeared in focal regions at the cell periphery before spreading to the cell interior. Line-scan images showed the peripheral rise of [Ca2+]i led that at the center of the cell by 34 +/- 4 ms (mean +/- SE, n = 3). These data demonstrate that the t-tubular network ensures synchronous increases of [Ca2+]i throughout the cell during an action potential. In the absence of t tubules or when the number of sarcolemmal Ca2+ channels opened by membrane depolarization is greatly reduced, stimulated increases of [Ca2+]i can be observed to arise in focal regions of the cell.


1998 ◽  
Vol 124 (8) ◽  
pp. 1744-1750 ◽  
Author(s):  
Kimihiro Yoshimoto ◽  
Yuichi Hattori ◽  
Hideki Houzen ◽  
Morio Kanno ◽  
Keishu Yasuda

2000 ◽  
Vol 23 (11P2) ◽  
pp. 1812-1815 ◽  
Author(s):  
BODO BRANDTS ◽  
MARC VAN BRACHT ◽  
FRANK TÜTTELMANN ◽  
MAURITZ A. ALLESSIE ◽  
HANS-JOACHIM TRAPPE

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.


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