Demonstration of anionic sites in rat myocardium and isolated cardiac myocytes with polyethylenimine

1986 ◽  
Vol 18 ◽  
pp. 3-3
Author(s):  
P KIRCHNER ◽  
J SCHAPER
Keyword(s):  
Cardiac Myocytes ◽  
Rat Myocardium ◽  
Anionic Sites ◽  
Isolated Cardiac Myocytes

l-Arginine ameliorates effects of ischemia and reperfusion in isolated cardiac myocytes

2003 ◽  
Vol 476 (1-2) ◽  
pp. 45-54 ◽  
Author(s):  
Adrian Au ◽  
William E. Louch ◽  
Gregory R. Ferrier ◽  
Susan E. Howlett
Keyword(s):  
Cardiac Myocytes ◽  
Ischemia And Reperfusion ◽  
Isolated Cardiac Myocytes

Differential effects of phospholamban and Ca2+/calmodulin-dependent kinase II on [Ca2+]i transients in cardiac myocytes at physiological stimulation frequencies

2008 ◽  
Vol 294 (5) ◽  
pp. H2352-H2362 ◽  
Author(s):  
Andreas A. Werdich ◽  
Eduardo A. Lima ◽  
Igor Dzhura ◽  
Madhu V. Singh ◽  
Jingdong Li ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Sarcoplasmic Reticulum ◽  
Cardiac Myocytes ◽  
Wild Type ◽  
Dependent Protein Kinase ◽  
Frequency Dependent ◽  
Physiological Range ◽  
Dependent Protein ◽  
Isolated Cardiac Myocytes

In cardiac myocytes, the activity of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is hypothesized to regulate Ca2+ release from and Ca2+ uptake into the sarcoplasmic reticulum via the phosphorylation of the ryanodine receptor 2 and phospholamban (PLN), respectively. We tested the role of CaMKII and PLN on the frequency adaptation of cytosolic Ca2+ concentration ([Ca2+]i) transients in nearly 500 isolated cardiac myocytes from transgenic mice chronically expressing a specific CaMKII inhibitor, interbred into wild-type or PLN null backgrounds under physiologically relevant pacing conditions (frequencies from 0.2 to 10 Hz and at 37°C). When compared with that of mice lacking PLN only, the combined chronic CaMKII inhibition and PLN ablation decreased the maximum Ca2+ release rate by more than 50% at 10 Hz. Although PLN ablation increased the rate of Ca2+ uptake at all frequencies, its combination with CaMKII inhibition did not prevent a frequency-dependent reduction of the amplitude and the duration of the [Ca2+]i transient. High stimulation frequencies in the physiological range diminished the effects of PLN ablation on the decay time constant and on the maximum decay rate of the [Ca2+]i transient, indicating that the PLN-mediated feedback on [Ca2+]i removal is limited by high stimulation frequencies. Taken together, our results suggest that in isolated mouse ventricular cardiac myocytes, the combined chronic CaMKII inhibition and PLN ablation slowed Ca2+ release at physiological frequencies: the frequency-dependent decay of the amplitude and shortening of the [Ca2+]i transient occurs independent of chronic CaMKII inhibition and PLN ablation, and the PLN-mediated regulation of Ca2+ uptake is diminished at higher stimulation frequencies within the physiological range.

scholarly journals The kinetics of transport of lactate and pyruvate into isolated cardiac myocytes from guinea pig. Kinetic evidence for the presence of a carrier distinct from that in erythrocytes and hepatocytes

1989 ◽  
Vol 264 (2) ◽  
pp. 409-418 ◽  
Author(s):  
R C Poole ◽  
A P Halestrap ◽  
S J Price ◽  
A J Levi
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Silicone Oil ◽  
Free Acid ◽  
Competitive Inhibitor ◽  
Isolated Cardiac Myocytes ◽  
Lactate And Pyruvate ◽  
Time Courses ◽  
Kinetics Of

1. Time courses for the uptake of L-lactate, D-lactate and pyruvate into isolated cardiac ventricular myocytes from guinea pig were determined at 11 degrees C or 0 degrees C (for pyruvate) in a citrate-based buffer by using a silicone-oil-filtration technique. These conditions enabled initial rates of transport to be measured without interference from metabolism of the substrates. 2. At a concentration of 0.5 mM, transport of all these substrates was inhibited by approx. 90% by 5 mM-alpha-cyano-4-hydroxycinnamate; at 10 mM-L-lactate a considerable portion of transport could not be inhibited. 3. Initial rates of L-lactate and pyruvate uptake in the presence of 5 mM-alpha-cyano-4-hydroxycinnamate were linearly related to the concentration of the monocarboxylate and probably represented diffusion of the free acid. The inhibitor-sensitive component of uptake obeyed Michaelis-Menten kinetics, with Km values for L-lactate and pyruvate of 2.3 and 0.066 mM respectively. 4. Pyruvate and D-lactate inhibited the transport of L-lactate, with Ki values (competitive) of 0.077 and 6.6 mM respectively; the Ki for pyruvate was very similar to its Km for transport. The Ki for alpha-cyano-4-hydroxycinnamate as a non-competitive inhibitor was 0.042 mM. 5. These results indicate that L-lactate, D-lactate and pyruvate share a common carrier in guinea-pig cardiac myocytes; the low stereoselectivity for L-lactate over D-lactate and the high affinity for pyruvate distinguish it from the carrier in erythrocytes and hepatocytes. The metabolic roles for this novel carrier in heart are discussed.

Abstract 1076: Conditional Fkbp12.6 Overexpression In Mouse Cardiac Myocytes Protects From Triggered Ventricular Arrhythmia Through Specific Alteration In Ec Coupling

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Barnabas Gellen ◽  
Ana-Maria Gomez ◽  
Khai Le Quang ◽  
Francois Briec ◽  
Laurent Vinet ◽  
...  
Keyword(s):  
Cardiac Myocytes ◽  
Antiarrhythmic Effect ◽  
Adrenergic Stimulation ◽  
Patch Clamp Technique ◽  
Ec Coupling ◽  
Before And After ◽  
Isolated Cardiac Myocytes ◽  
Pre Treatment ◽  
Specific Alteration ◽  
Ventricular Tachycardias

In cardiac myocytes, Ca2+ release from the sarcoplasmic reticulum (SR) into the cytoplasm via the ryanodine receptor (RyR2) activates cell contraction. During diastole, RyR2 are closed and prevent Ca2+ efflux from the SR. One of the major regulators of RyR2 function is FKBP12.6. Binding of FKBP12.6 stabilizes RyR2 in the closed formation in diastole and contributes to synchronized RyR2 opening in systole. Beta-adrenergic stimulation dissociates FKBP12.6 from RyR2, leading to diastolic Ca2+ leak that can trigger ventricular tachycardias (VT). We tested the hypothesis whether FKBP12.6 overexpression in the myocardium can reduce the susceptibility to VT in stress conditions. We developed a mouse model with conditional cardiac specific overexpression of FKBP12.6 using the Tet-Off system. Transgenic (TG) mice and controls (CT) were examined by echocardiography, PV-catheterization, ECG, and underwent intracardiac stimulation to trigger VT before and after pre-treatment with isoproterenol. In isolated cardiac myocytes, SR Ca2+ load, Ca2+ sparks and Ca2+ transient were measured using confocal microscopy, and L-type Ca2+ current was determined by the patch-clamp technique. Echocardiography, PV-catheterization and ECG recording did not reveal differences between Tg (n=11) and CT (n=13) mice. Burst pacing (figure 1) could induce TV in 4 of 24 controls and in 0 of 14 TG mice (n.s.). Following pre-treatment with isoproterenol, TV could be induced in 10 of 23 controls, but only in 1 of 14 TG animals (figure 2, p<0.05). In isolated myocytes, decreased Ca2+ spark frequency, increased Ca2+ spark size, unchanged SR Ca2+ load and decreased Ca2+ transient were observed in TG cells (n=19) as compared to controls (n=48, p<0.05). L-type Ca2+ channel current was found to be decreased in Tg myocytes (n=29 vs n=32, p<0.01). We conclude that myocardial FKBP12.6 overexpression has a protective effect against VT induced by rapid pacing after pretreatment with catecholamines. This antiarrhythmic effect is probably, at least in part, linked to decreased diastolic SR Ca2+ leak. Our results support the hypothesis that increased FKBP12.6 binding to RyR2 might represent a potential therapeutical target in the prevention and treatment of ventricular arrhythmias.

Superoxide dismutase: tissue, cellular, and subcellular distribution in adult canine heart

1985 ◽  
Vol 249 (5) ◽  
pp. C379-C384 ◽  
Author(s):  
A. M. Spanier ◽  
W. B. Weglicki ◽  
D. L. Stiers ◽  
H. P. Misra
Keyword(s):  
Cardiac Myocytes ◽  
Cardiac Myocyte ◽  
Mitochondrial Fraction ◽  
Retardation Factor ◽  
Myocardial Tissue ◽  
Canine Heart ◽  
Sod Activity ◽  
Mitochondrial Fractions ◽  
Isolated Cardiac Myocytes ◽  
Moving Band

Cell-free extracts of canine myocardial tissue were found to contain two biochemically and electrophoretically distinct superoxide dismutases (SOD), an enzyme that provides defense against the deleterious effect of superoxide radicals (O2.-). Polyacrylamide gel (7.5%) electrophoresis revealed two distinct bands of SOD activity: a slower moving band [retardation factor (Rf) = 0.4] resembling the manganese SOD found in bacteria and mitochondria (which is not inhibited by 2.5 mM cyanide) and a faster moving band (Rf = 0.75) that is sensitive to cyanide. In contrast, extracts from isolated adult canine cardiac myocytes were found to contain only the cyanide-insensitive SOD. Extracts of whole myocardium and isolated cardiac myocytes contain 22.3 +/- 1.2 and 27.0 +/- 1.5 U cyanide-insensitive SOD/mg protein, respectively. However, the activity of cyanide-sensitive SOD in these fractions is 7.9 +/- 2.0 (tissue) and 1.5 +/- 1.4 (cells) U/mg protein. Cardiac myocyte SOD activity was particulate in nature, and the major part of the SOD activity was associated with heavy mitochondrial fractions. The biologic significance of this higher activity of SOD in the heavier mitochondrial fraction remains to be elucidated.

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