scholarly journals SELECTIVE DEPOSITION OF LANTHANUM IN MAMMALIAN CARDIAC CELL MEMBRANES

1973 ◽  
Vol 58 (1) ◽  
pp. 1-10 ◽  
Author(s):  
A. Martinez-Palomo ◽  
D. Benitez ◽  
J. Alanis

Perfusion of beating false tendons of the dog heart with ionic lanthanum produced drastic but reversible modifications of the excitability and the transmembrane action potential of Purkinje cells. Ultrastructural examination of these cells revealed the appearance of a fine extracellular precipitate detectable on unstained sections. In addition, specimens perfused with La+++ showed a striking increase in the contrast of the sarcolemma, particularly in gap junctions and in pinocytic vesicles. La+++ deposits were restricted to the cytoplasmic leaflets of the sarcolemma; no precipitates were found at the plasma membrane of fibroblasts, endothelial and smooth muscle cells, or unmyelinated nerve fibers present in the same specimens. A selective deposition of La+++ was also observed in the sarcolemma of atrial and ventricular cells of dog, rabbit, and cat hearts, as well as in the membrane of the transverse tubular system of ventricular cells. Both the electrophysiological effects and the ultrastructural membrane deposits produced by La+++ disappeared when the specimens were subsequently perfused with phosphate-containing tyrode solution. These results tend to demonstrate that a distinctive feature of the sarcolemma of mammalian cardiac cells is the presence of regions with a high surface density of binding sites for polyvalent cations.

1970 ◽  
Vol 48 (4) ◽  
pp. 837-839 ◽  
Author(s):  
Haukur Melax ◽  
Thomas S. Leeson

The sinoatrial node of the rat is composed of loosely interwoven modified cardiac muscle cells, which are lined up in groups to form somewhat irregular layers or plates. A generous amount of atrial specific granules is found in their cytoplasm. Between the nodal cells there is a loose connective tissue containing numerous bundles of unit fibrils of collagen and unmyelinated nerve fibers. In the atrioventricular node the modified cardiac cells are larger than those of the sinoatrial node, and are arranged in small groups. They contain a large amount of glycogen. Unmyelinated nerve fibers are extremely numerous in the atrioventricular node and myelinated nerve fibers are also present.


2004 ◽  
Vol 286 (4) ◽  
pp. H1300-H1309 ◽  
Author(s):  
Hanne Borger Rasmussen ◽  
Morten Møller ◽  
Hans-Günther Knaus ◽  
Bo Skaaning Jensen ◽  
Søren-Peter Olesen ◽  
...  

In the heart, several K+ channels are responsible for the repolarization of the cardiac action potential, including transient outward and delayed rectifier K+ currents. In the present study, the cellular and subcellular localization of the two delayed rectifier K+ channels, KCNQ1 and ether- a- go- go-related gene-1 (ERG1), was investigated in the adult rat heart. Confocal immunofluorescence microscopy of atrial and ventricular cells revealed that whereas KCNQ1 labeling was detected in both the peripheral sarcolemma and a structure transversing the myocytes, ERG1 immunoreactivity was confined to the latter. Immunoelectron microscopy of atrial and ventricular myocytes showed that the ERG1 channel was primarily expressed in the transverse tubular system and its entrance, whereas KCNQ1 was detected in both the peripheral sarcolemma and in the T tubules. Thus, whereas ERG1 displays a very restricted subcellular localization pattern, KCNQ1 is more widely distributed within the cardiac cells. The localization of these K+ channels to the transverse tubular system close to the Ca2+ channels renders them with maximal repolarizing effect.


2002 ◽  
Vol 282 (3) ◽  
pp. H1007-H1017 ◽  
Author(s):  
Thomas Zimmer ◽  
Christian Bollensdorff ◽  
Volker Haufe ◽  
Eckhard Birch-Hirschfeld ◽  
Klaus Benndorf

We isolated two full-length cDNA clones from the adult murine heart that encode two different voltage-gated Na+ channels: mH1 and mH2. Sequence comparisons indicated that mH1 is highly homologous to rat SCN5A, whereas mH2 is highly homologous to SCN4A, expressed in rat skeletal muscle. Electrophysiological properties of mH1 channels strongly resembled the tetrodotoxin (TTX)-resistant Na+ current of mouse ventricular cells, whereas mH2 channels activated at more positive potentials and were highly sensitive to TTX [50% inhibitory constant (IC50) = 11 nM]. We found that mH2 is not expressed in cardiac cells of neonatal mice, but appears to be upregulated during the development. Besides these Na+channel isoforms, we also detected two alternatively spliced mH1 variants that were characterized by deletions within the sequence coding for the intracellular loop between domains II and III. One of the shortened channels, mH1–2, developed Na+ currents indistinguishable from those of mH1. The other splice variant (mH1–3) did not form functional channels. Quantitative reverse transcriptase-polymerase chain reaction indicated that RNA preparations of the adult mouse heart contain 54% mH1, 25% mH1–2, 16% mH2, and 5% mH1–3. Conclusively, mH1 generates the main portion of the mouse cardiac TTX-resistant Na+ current and mH2 is a candidate for TTX-sensitive currents previously described in adult cardiomyocytes. Furthermore, the presence of mH1–2 and mH1–3 transcripts indicates that alternative splicing plays a role in the regulation of functional Na+ channels in cardiomyocytes.


1987 ◽  
Vol 67 (3) ◽  
pp. A276-A276
Author(s):  
Robert R. Myers ◽  
Michael W. Kalichman ◽  
Henry C. Powell

1973 ◽  
Vol 76 (3) ◽  
pp. 1004-1007 ◽  
Author(s):  
A. V. Zeveke ◽  
V. I. Myaderov ◽  
V. A. Utkin ◽  
V. L. Shaposhnikov

1996 ◽  
Vol 271 (3) ◽  
pp. H896-H905 ◽  
Author(s):  
S. J. Sollott ◽  
B. D. Ziman ◽  
D. M. Warshaw ◽  
H. A. Spurgeon ◽  
E. G. Lakatta

We sought to determine whether resting or diastolic cardiac myocyte length during low stimulation rates is regulated by myofilament interaction. Cytosolic Ca2+ concentration ([Ca2+]i, via indo 1 fluorescence) and length, in the presence and absence of 2,3-butanedione monoxime (BDM), a potent inhibitor of force production in striated muscle, were measured in rat and guinea pig cardiac myocytes at rest and after electrical stimulation. In tetanized cells BDM reduced steady contraction amplitudes for a given [Ca2+]i. In an actomyosin-sliding filament assay without Ca2+ or regulatory proteins, BDM decreased actin filament velocity along myosin. BDM increased both diastolic and resting cell lengths without changes in [Ca2+]i. The resting cell length also increased when [Ca2+]i was reduced by removing extracellular Ca2+, an effect further enhanced by BDM and by loading cells with the intracellular Ca2+ chelator, 1,2-bis(2-amino-phenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethylester. Thus myofilament interaction is present in cardiac cells, both at rest or during low rates of stimulation, and this myofilament interaction is regulated, in part, by the ambient [Ca2+]i.


2005 ◽  
Vol 98 (6) ◽  
pp. 2328-2336 ◽  
Author(s):  
Chae-Ryon Kong ◽  
Nenad Bursac ◽  
Leslie Tung

Although the prevailing view of mechanoelectric feedback (MEF) in the heart is in terms of longitudinal cell stretch, other mechanical forces are considerable during the cardiac cycle, including intramyocardial pressure and shear stress. Their contribution to MEF is largely unknown. In this study, mechanical stimuli in the form of localized fluid jet pulses were applied to neonatal rat ventricular cells cultured as confluent monolayers. Such pulses result in pressure and shear stresses (but not longitudinal stretch) in the monolayer at the point of impingement. The goal was to determine whether these mechanical stimuli can trigger excitation, initiate a propagated wave, and induce reentry. Cells were stained with the voltage-sensitive dye RH237, and multi-site optical mapping was used to record the spread of electrical activity in isotropic and anisotropic monolayers. Pulses (10 ms) with velocities ranging from 0.3 to 1.8 m/s were applied from a 0.4-mm diameter nozzle located 1 mm above the cell monolayer. Fluid jet pulses resulted in circular wavefronts that propagated radially from the stimulus site. The likelihood for mechanical stimulation was quantified as an average stimulus success rate (ASSR). ASSR increased with jet amplitude and time waited between stimuli and decreased with the application of gadolinium and streptomycin, blockers of stretch-activated channels, but not with nifedipine, a blocker of the L-type Ca channel. Absence of cellular injury was confirmed by smooth propagation maps and propidium iodide stains. In rare instances, the mechanical pulse resulted in the induction of reentrant activity. We conclude that mechanical stimuli other than stretch can evoke action potentials, propagated activity, and reentrant arrhythmia in two-dimensional sheets of cardiac cells.


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