Characterization of contractions in enzymatically isolated rat ventricular myocytes: effects of ouabain and rubidium

1984 ◽  
Vol 62 (3) ◽  
pp. 253-258 ◽  
Author(s):  
Matti Vornanen
Keyword(s):  
Sodium Pump ◽  
Ventricular Myocytes ◽  
Contractile Activity ◽  
Full Effect ◽  
Pump Activity ◽  
Sodium Pump Inhibition ◽  
Beating Frequency ◽  
Stimulation Of

The role of sarcolemma and especially sodium pump activity in the control of phasic contractile activity of Ca2+ tolerant myocytes was studied using ouabain and rubidium as sodium pump inhibitors. Initially, ouabain increased both the amplitude of shortening and the frequency of phasic contractions. Later, the amplitude began to decline whereas the frequency of beating continued to rise, often terminating in a steady contracture of the myocyte. Rubidium caused a rapid rise of beating frequency, which reached its full effect within 1–5 min and remained steady after that. The stimulation of contraction frequency and the inhibition of Na+–K+ ATPase were correlated in the case of ouabain but not in the case of rubidium. The results suggest that the stimulation of phasic contractions may be caused by increased uptake of cellular calcium through Na+–Ca+ exchange as a consequence of sodium pump inhibition and (or) depolarization of the sarcolemma by ouabain and rubidium.

Protein kinase Cε and the antiadrenergic action of adenosine in rat ventricular myocytes

2004 ◽  
Vol 287 (4) ◽  
pp. H1721-H1729 ◽  
Author(s):  
Koji Miyazaki ◽  
Satoshi Komatsu ◽  
Mitsuo Ikebe ◽  
Richard A. Fenton ◽  
James G. Dobson
Keyword(s):  
Electrical Stimulation ◽  
Protein Kinase ◽  
Ventricular Myocytes ◽  
Adrenergic Agonist ◽  
Inhibitory Peptide ◽  
Rat Ventricular Myocytes ◽  
Adult Rat ◽  
Tubular System ◽  
Stimulation Of

Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A1 receptors (A1R). The role of PKCε in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKCε was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKCε construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKCε was found localized primarily in transverse tubules. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 μM rendered an enhanced localization of PKCε in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 μM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKCε overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKCε inhibitory peptide. These results suggest that the translocation of PKCε to the t-tubular system plays an important role in A1R-mediated antiadrenergic actions in the heart.

Exercise and glycogen depletion: effects on ability to activate muscle phosphorylase

1986 ◽  
Vol 60 (5) ◽  
pp. 1518-1523 ◽  
Author(s):  
S. H. Constable ◽  
R. J. Favier ◽  
J. O. Holloszy
Keyword(s):  
Muscle Contraction ◽  
Muscle Glycogen ◽  
Contractile Activity ◽  
Strenuous Exercise ◽  
Glycogen Depletion ◽  
Significant Difference ◽  
Muscle Phosphorylase ◽  
Glycogen Repletion ◽  
Stimulation Of

Phosphorylase activation reverses during prolonged contractile activity. Our first experiment was designed to determine whether this loss of ability to activate phosphorylase by stimulation of muscle contraction persists following exercise. Phosphorylase activation by stimulation of muscle contraction was markedly inhibited in rats 25 min after exhausting exercise. To evaluate the role of glycogen depletion, we accelerated glycogen utilization by nicotinic acid administration. A large difference in muscle glycogen depletion during exercise of the same duration did not influence the blunting of phosphorylase activation. Phosphorylase activation by stimulation of contraction was more severely inhibited following prolonged exercise than after a shorter bout of exercise under conditions that resulted in the same degree of glycogen depletion. A large difference in muscle glycogen repletion during 90 min of recovery was not associated with a significant difference in the ability of muscle stimulation to activate phosphorylase, which was still significantly blunted. Phosphorylase activation by epinephrine was also markedly inhibited in muscle 25 min after strenuous exercise but had recovered completely in glycogen-repleted muscle 90 min after exercise. These results provide evidence that an effect of exercise other than glycogen depletion is involved in causing the inhibition of phosphorylase activation; however, they do not rule out the possibility that glycogen depletion also plays a role in this process.

scholarly journals Role of sodium pump activity in warm induction of cardioplegia combined with reperfusion of oxygenated cardioplegic solution

1995 ◽  
Vol 110 (1) ◽  
pp. 103-110 ◽  
Author(s):  
Tokumitsu Ko ◽  
Hajime Otani ◽  
Hiroji Imamura ◽  
Kyoko Omori ◽  
Chiyoko Inagaki
Keyword(s):  
Sodium Pump ◽  
Cardioplegic Solution ◽  
Pump Activity

scholarly journals Esophagus: serotoninerdgic regulation

2020 ◽  
pp. 137-142
Author(s):  
A. M. Puzikov
Keyword(s):  
Serotonin Receptors ◽  
Contractile Activity ◽  
Smooth Muscles ◽  
Emg Activity ◽  
Enhancing Effect ◽  
Adventitial Layer ◽  
Important Player ◽  
Ganglion Neurons ◽  
Stimulation Of

Introduction: Serotonin (5-hydroxytryptamine, 5-HT) is a regulatory neurotransmitter and a hormone in the CNS and hole organs, the esophagus including. It is known that serotonin, activating its own receptors, stimulates contractile activity of the esophageal muscles. However, role of different type receptors in the 5-HT induced contractile activity of the esophagus is insufficiently known.The aim: — to determine which type of 5-HT receptors mediate serotonin dependent contractile activity of the esophagus.Material and methods: This is a electromyography study of rat esophagus contractile activity under serotonin stimulation of 5-HT3,4 and 5-HT2,1 receptors separately modulated. The role of different serotonin receptors in the 5-HT induced contractile activity of the esophagus was evaluated by measuring the amplitude and frequency of the slow wave electromyogram (EMG) by the noninvasive microelectrodes imposed on the adventitial layer of the esophagus.Results: Administration of the 5-HT3,4 receptors inhibitors excluded caused by serotonin the increment of EMG activity of the contractile activity of the esophagus. Administration of the 5-HT1,2 receptors inhibitors blocked the serotonin enhanced EMG activity of the esophagus.Conclusion: Our results indicate that serotonin is the important player in the regulation of the rat's esophagus contractility; 5-HT enhancing effect on contraction of the esophageal smooth muscles is mediated through the activation of 5-HT1,2 receptors expressed on the smooth muscle cells, and by activation of 5-HT3,4 receptors expressed on the ganglion neurons.

Sodium Pump Activity in Uremic Erythrocytes: A Microcalorimetric Study

1992 ◽  
Vol 15 (3) ◽  
pp. 135-138 ◽  
Author(s):  
P. Gallice ◽  
H. Kovacic ◽  
M. Baz ◽  
Y. Berland ◽  
R. Elsen ◽  
...  
Keyword(s):  
Heat Production ◽  
Healthy Subjects ◽  
Sodium Pump ◽  
Age Distribution ◽  
Lower Activity ◽  
Flow Microcalorimetry ◽  
Pump Activity ◽  
Uremic Patients ◽  
The Difference ◽  
Sodium Pump Inhibition

Erythrocyte thermogenesis was studied by flow microcalorimetry in 25 healthy subjects and 27 uremic patients. The heat production (HP) from cells in plasma, decrease in HP induced by ouabain (a specific sodium pump inhibitor) and index of rate response to ouabain action were measured. HP was higher in uremic patients than controls. Sodium pump inhibition with ouabain induced the same decrease in HP in the two groups. The index of rate response to ouabain action was lower in uremic patients than in controls. The difference in total HP may be due to a different age distribution of erythrocytes. Mean sodium pump activity was identical in the two groups, but some patients had lower activity than controls. Ouabain seems to act more slowly in many patients than in controls, perhaps because of hindered binding of the inhibitor.

The functional role of cardiac T-tubules explored in a model of rat ventricular myocytes

2006 ◽  
Vol 364 (1842) ◽  
pp. 1187-1206 ◽  
Author(s):  
Michal Pásek ◽  
Jiři Šimurda ◽  
Georges Christé
Keyword(s):  
Ventricular Myocytes ◽  
Contractile Activity ◽  
Tubular Lumen ◽  
Current Clamp Mode ◽  
Intracellular Ca ◽  
Ionic Changes ◽  
Access Resistance ◽  
T Tubules ◽  
Tubular Membranes

The morphology of the cardiac transverse-axial tubular system (TATS) has been known for decades, but its function has received little attention. To explore the possible role of this system in the physiological modulation of electrical and contractile activity, we have developed a mathematical model of rat ventricular cardiomyocytes in which the TATS is described as a single compartment. The geometrical characteristics of the TATS, the biophysical characteristics of ion transporters and their distribution between surface and tubular membranes were based on available experimental data. Biophysically realistic values of mean access resistance to the tubular lumen and time constants for ion exchange with the bulk extracellular solution were included. The fraction of membrane in the TATS was set to 56%. The action potentials initiated in current-clamp mode are accompanied by transient K + accumulation and transient Ca 2+ depletion in the TATS lumen. The amplitude of these changes relative to external ion concentrations was studied at steady-state stimulation frequencies of 1–5 Hz. Ca 2+ depletion increased from 7 to 13.1% with stimulation frequency, while K + accumulation decreased from 4.1 to 2.7%. These ionic changes (particularly Ca 2+ depletion) implicated significant decrease of intracellular Ca 2+ load at frequencies natural for rat heart.

Pharmacological Characterization of an Adenylyl Cyclase-Coupled 5-HT Receptor in Aplysia: Comparison With Mammalian 5-HT Receptors

2003 ◽  
Vol 89 (3) ◽  
pp. 1440-1455 ◽  
Author(s):  
Jonathan E. Cohen ◽  
Chiadi U. Onyike ◽  
Virginia L. McElroy ◽  
Allison H. Lin ◽  
Thomas W. Abrams
Keyword(s):  
Adenylyl Cyclase ◽  
Rank Order ◽  
Physiological Saline ◽  
Receptor Subtypes ◽  
Pharmacological Profile ◽  
Pharmacological Characterization ◽  
Firing Properties ◽  
Stimulation Of

We attempted to identify compounds that are effective in blocking the serotonin (5-hydroxytryptamine, 5-HT) receptor(s) that activate adenylyl cyclase (AC) in Aplysia CNS. We call this class of receptor 5-HTapAC. Eight of the 14 antagonists tested were effective against 5-HTapAC in CNS membranes with the following rank order of potency: methiothepin > metergoline ∼ fluphenazine > clozapine > cyproheptadine ∼ risperidone ∼ ritanserin > NAN-190. GR-113808, olanzapine, Ro-04-6790, RS-102221, SB-204070, and spiperone were inactive. Methiothepin completely blocked 5-HT stimulation of AC with a K b of 18 nM. Comparison of the pharmacological profile of the 5-HTapAC receptor with those of mammalian 5-HT receptor subtypes suggested it most closely resembles the 5-HT6 receptor. AC stimulation in Aplysia sensory neuron (SN) membranes was also blocked by methiothepin. Methiothepin substantially inhibited two effects of 5-HT on SN firing properties that are mediated by a cAMP-dependent reduction in S-K+ current: spike broadening in tetraethylammonium/nifedipine and increased excitability. Consistent with cyproheptadine blocking 5-HT stimulation of AC, cyproheptadine also blocked the 5-HT-induced increase in SN excitability. Methiothepin was less effective in blocking AC-mediated modulatory effects of 5-HT in electrophysiological experiments on SNs than in blocking AC stimulation in CNS or SN membranes. This reduction in potency appears to be due to effects of the high ionic strength of physiological saline on the binding of this antagonist to the receptor. Methiothepin also antagonized AC-coupled dopamine receptors but not AC-coupled small cardioactive peptide receptors. In conjunction with other pharmacological probes, this antagonist should be useful in analyzing the role of 5-HT in various forms of neuromodulation in Aplysia.

scholarly journals Glucagon stimulation of hepatic Na+-pump activity and α-subunit phosphorylation in rat hepatocytes

1996 ◽  
Vol 313 (3) ◽  
pp. 983-989 ◽  
Author(s):  
Christopher J. LYNCH ◽  
Kenneth M. McCALL ◽  
Yuk-Chow NG ◽  
Stacy A. HAZEN
Keyword(s):  
Protein Kinase ◽  
Rat Kidney ◽  
Rat Hepatocytes ◽  
Transport Activity ◽  
Isolated Rat Hepatocytes ◽  
Α Subunit ◽  
Na Pump ◽  
Pump Activity ◽  
Stimulation Of

In this study the possible role of Na+ influx, arachidonate mediators and α-subunit phosphorylation in the stimulatory response of hepatic Na+/K+-ATPase to glucagon was examined. Glucagon stimulation of ouabain-sensitive 86Rb+ uptake in freshly isolated rat hepatocytes reached maximal levels in less than 1 min after hormone addition and was half-maximal (EC50) at a concentration of 2.4(±1.3)×10-10 M. Analysis of the K+-dependence of this response indicates an effect on the apparent Vmax. for K+ with no significant change in the apparent K0.5. Unlike monensin, glucagon stimulation of Na+/K+-ATPase-mediated transport activity was not associated with an increase in 22Na+ influx. This indicates that the stimulation of Na+/K+-ATPase by glucagon is not secondary to an increase in Na+ influx. A role for arachidonate mediators in this effect also appears unlikely because neither basal nor glucagon-stimulated ouabain-sensitive 86Rb+ uptake was significantly affected by supramaximal concentrations of cyclo-oxygenase, lipoxygenase, cytochrome P-450 or phospholipase A2 inhibitors. To study the possible role of protein kinase-mediated phosphorylation in the stimulation of ouabain-sensitive 86Rb+ uptake, hepatocytes were metabolically radiolabelled with [32P]Pi. Glucagon stimulated incorporation of 32P into a 95 kDa phosphoprotein that co-migrates with Na+/K+-ATPase α-subunit immunoreactivity in two-dimensional gel electrophoresis. The α-subunit could be immunoprecipitated from detergent-solubilized particulate fractions of hepatocytes using an anti-(rat kidney Na+/K+-ATPase) serum. When hepatocytes were metabolically radiolabelled with [32P]Pi, the immunoprecipitated α-subunit contained 32P. Glucagon increased the incorporation of 32P into the immunoprecipitated subunit by 197±21% (n = 6). Similar results were observed with a rabbit anti-peptide serum (‘anti-LEAVE’ serum) prepared against an amino acid sequence in the α-subunit. The EC50 for glucagon-stimulated phosphorylation of the α-subunit (1×10-10 M) was very close to that for glucagon stimulation of ouabain-sensitive 86Rb+ uptake. In conclusion, it appears that glucagon stimulation of hepatic Na+/K+-ATPase-mediated transport activity is not secondary to increases in Na+ influx or changes in the levels of an arachidonate mediator. The data provide support for the hypothesis that glucagon stimulation of Na+-pump activity in hepatocytes may be related to protein kinase-mediated changes in the phosphorylation state of the α-subunit.

Sign in / Sign up

Export Citation Format

Share Document