Interaction of sodium with the sarcolemmal calcium system

1978 ◽  
Vol 56 (1) ◽  
pp. 1-6 ◽  
Author(s):  
N. C. Morcos ◽  
A. L. Jacobson
Keyword(s):  
Guinea Pig ◽  
Atpase Activity ◽  
Intracellular Calcium ◽  
Calcium Binding ◽  
Cardiac Glycosides ◽  
Dependent Manner ◽  
Sodium Ions ◽  
Subsequent Increase ◽  
Guinea Pig Heart ◽  
Binding Process

Sarcolemma isolated from guinea pig heart binds calcium in an ATP-dependent manner. Sodium ions decrease the total amount of calcium bound by the membranes. ATP-dependent calcium binding is more sensitive to sodium than the non-ATP-dependent calcium binding. The ATPase active during calcium binding is affected by sodium ions to the same extent as the ATP-dependent calcium binding process. The inhibition of the calcium binding process and of ATPase activity by sodium was more pronounced when the membranes were preincubated with sodium. The effect of sodium on calcium binding is dependent on both the time of contact between sodium and the membranes and the concentration of sodium. It is suggested that the effect of sodium on the calcium binding system in the sarcolemma may be a link between the inhibition of Na+K+-ATPase (EC 3.6.1.3) by cardiac glycosides and the subsequent increase in intracellular calcium.

Ultrastructural and enzymatic development of fetal guinea pig heart

1982 ◽  
Vol 243 (1) ◽  
pp. H87-H93 ◽  
Author(s):  
T. P. Rolph ◽  
C. T. Jones ◽  
D. Parry
Keyword(s):  
Guinea Pig ◽  
Atpase Activity ◽  
Enzyme Activities ◽  
Citric Acid Cycle ◽  
Acid Metabolism ◽  
Fetal Heart ◽  
Glycolytic Enzyme ◽  
Guinea Pig Heart ◽  
Threefold Increase ◽  
Phosphofructokinase Activity

The activities of some enzymes of glycolysis, the citric acid cycle, and amino acid metabolism have been measured in the fetal guinea pig heart over the last third of gestation and correlated with heart ultrastructural development. There is little change in glycolytic enzyme activity except for a two- to threefold increase in phosphofructokinase activity. Mitochondrial content and enzyme activities are low in the early fetal heart, and, although content is similar in the late fetus and adult, enzyme activities increase twofold postnatally, indicating fetal heart mitochondria are incompletely developed. The activities of aspartate and particularly alanine aminotransferase are low in the fetal heart. Over the last third of gestation the myofibrillar content of the fetal myocyte increases twofold to the adult value by term. Associated with this is a fourfold rise in myofibrillar and sarcoplasmic reticulum Ca2+-ATPase activity. Na+-K+-ATPase activity is similar in the late fetal and adult heart but one-third lower in the early fetal heart.

Ouabain potentiation and Ca release from sarcoplasmic reticulum in cardiac and skeletal muscle cells

1982 ◽  
Vol 60 (4) ◽  
pp. 542-555 ◽  
Author(s):  
S. Fujino ◽  
M. Fujino
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Skeletal Muscles ◽  
Cardiac Glycosides ◽  
Positive Inotropic Effect ◽  
Frog Heart ◽  
Heart Ventricle ◽  
Guinea Pig Heart ◽  
Intracellular Mechanism ◽  
Cat Heart

In this article, we describe a possible mechanism of ouabain potentiation in heart based on the following findings in cardiac and skeletal muscles of various species. (1) In heart ventricle muscles of frog and guinea pig, the ouabain potentiation is produced without an effect on Ca influx. In both frog and cat heart ventricle muscles, ouabain potentiates the rapid cooling contracture with or without caffeine in a Ca-deprived medium. It follows, therefore, that the ouabain potentiation is produced by an "intracellular" mechanism. (2) In crab single muscle fibers, contractile responses such as twitch, potassium-induced contracture, caffeine-induced contracture, and water-induced contracture are remarkably potentiated if ouabain is present within the fibers by microinjection, whereas the situation is reversed if the drug is given extracellularly. (3) The ouabain potentiated the Ca release from fragmented sarcoplasmic reticulum (FSR) isolated from cat, guinea pig, and frog heart and from skeletal muscles as a result of the procedures used, such as changing the ionic environment. (4) In frog, cat, and guinea pig heart ventricle muscles, a reduction of contractility as a result of pretreatment with urea–Ringer's was completely cancelled by ouabain almost without influencing the membrane depolarization. Based on these findings and others, the deduction was made that the positive inotropic effect of cardiac glycosides on the heart is brought about by potentiation of contraction – Ca release from the intracellular store sites, namely the sarcoplasmic reticulum.

Effect of doxorubicin on calcium binding sites in guinea-pig heart

1986 ◽  
Vol 35 (7) ◽  
pp. 1203-1204 ◽  
Author(s):  
Fabrizio Villani ◽  
Elena Monti ◽  
Francesco Piccinini ◽  
Luigia Favall ◽  
Annalinda Rozza Dionigi ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Binding Sites ◽  
Calcium Binding ◽  
Guinea Pig Heart ◽  
Calcium Binding Sites

Muscarinic inhibition of cardiac norepinephrine and neuropeptide Y release during ischemia and reperfusion

1994 ◽  
Vol 267 (6) ◽  
pp. R1552-R1558 ◽  
Author(s):  
A. Haunstetter ◽  
M. Haass ◽  
X. Yi ◽  
C. Kruger ◽  
W. Kubler
Keyword(s):  
Guinea Pig ◽  
Neuropeptide Y ◽  
Stellate Ganglion ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Muscarinic Agonists ◽  
Concentration Dependent Manner ◽  
Guinea Pig Heart ◽  
Specific Antagonist ◽  
Stop Flow

It was the aim of the present study to characterize the modulatory effect of muscarinic agonists on the overflow of norepinephrine and neuropeptide Y (NPY) from the in situ perfused guinea pig heart, induced by electrical stimulation of the left stellate ganglion (6 Hz, 5 V, 1 min). The muscarinic agonists oxotremorine (0.01-1 microM) and carbachol (0.1-10 microM) reduced norepinephrine and NPY overflow in a concentration-dependent manner to approximately 30% of control. The inhibitory effect of carbachol was antagonized by the unspecific muscarinic antagonist atropine (1 microM) but not by the nicotinic antagonist hexamethonium (100 microM). The M2-specific antagonist AF-DX-116BS was 25 times more potent than the M1-specific antagonist pirenzepine in antagonizing the inhibitory effect of carbachol [50% inhibitory concentration (IC50) = 0.2 microM for AF-DX-116BS; IC50 = 5.0 microM for pirenzepine]. These findings indicate that presynaptic muscarinic inhibition of stimulated norepinephrine and NPY release from the guinea pig heart is mediated mainly by activation of M2 receptors. As early as 2 min after stop-flow ischemia, the inhibitory effect of carbachol (10 microM) on the stimulation-evoked overflow of norepinephrine and NPY was lost. On reperfusion with oxygenated buffer after 10 min of stop-flow ischemia the inhibitory effect of carbachol (10 microM) on stimulation-induced norepinephrine and NPY overflow recovered within 3 min.

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