scholarly journals Oxidation Process of Adrenaline in Freshly Isolated Rat Cardiomyocytes: Formation of Adrenochrome, Quinoproteins, and GSH Adduct

2007 ◽  
Vol 20 (8) ◽  
pp. 1183-1191 ◽  
Author(s):  
Vera Marisa Costa ◽  
Renata Silva ◽  
Luísa Maria Ferreira ◽  
Paula Sério Branco ◽  
Félix Carvalho ◽  
...  
Keyword(s):  
Oxidation Process ◽  
Rat Cardiomyocytes ◽  
Isolated Rat

scholarly journals Oxidation process of adrenaline in freshly isolated rat cardiomyocytes: Formation of adrenochrome, quinoproteins and Gsh-adduct

2007 ◽  
Vol 172 ◽  
pp. S64
Author(s):  
Vera Costa ◽  
Renata Silva ◽  
Luísa Ferreira ◽  
Paula Branco ◽  
Félix Carvalho ◽  
...  
Keyword(s):  
Oxidation Process ◽  
Rat Cardiomyocytes ◽  
Isolated Rat

scholarly journals Adenoprotection of the heart involves phospholipase C-induced activation and translocation of PKC-ε to RACK2 in adult rat and mouse

2009 ◽  
Vol 297 (2) ◽  
pp. H718-H725 ◽  
Author(s):  
Richard A. Fenton ◽  
Satoshi Komatsu ◽  
Mitsuo Ikebe ◽  
Lynne G. Shea ◽  
James G. Dobson
Keyword(s):  
Confocal Microscopy ◽  
Phospholipase C ◽  
Adrenergic Agonist ◽  
Rat Cardiomyocytes ◽  
Scanning Confocal Microscopy ◽  
Adult Rat ◽  
Sds Page ◽  
T Tubules ◽  
Isolated Rat ◽  
Stimulation Of

Adenosine protects the heart from adrenergic overstimulation. This adenoprotection includes the direct anti-adrenergic action via adenosine A1 receptors (A1R) on the adrenergic signaling pathway. An indirect A1R-induced attenuation of adrenergic responsiveness involves the translocation of PKC-ε to t-tubules and Z-line of cardiomyocytes. We investigated with sarcomere imaging, immunocytochemistry imaging, and coimmunoprecipitation (co-IP) whether A1R activation of PKC-ε induces the kinase translocation to receptor for activated C kinase 2 (RACK2) in isolated rat and mouse hearts and whether phospholipase C (PLC) is involved. Rat cardiomyocytes were treated with the A1R agonist chlorocyclopentyladenosine (CCPA) and exposed to primary PKC-ε and RACK2 antibodies with secondaries conjugated to Cy3 and Cy5 (indodicarbocyanine), respectively. Scanning confocal microscopy showed that CCPA caused PKC-ε to reversibly colocalize with RACK2 within 3 min. Additionally, rat and mouse hearts were perfused and stimulated with CCPA or phenylisopropyladenosine to activate A1R, or with phorbol 12-myristate 13-acetate to activate PKC. RACK2 was immunoprecipitated from heart extracts and resolved with SDS-PAGE. Western blotting showed that CCPA, phenylisopropyladenosine, and phorbol 12-myristate 13-acetate in the rat heart increased the PKC-ε co-IP with RACK2 by 186, 49, and >1,000%, respectively. The A1R antagonist 8-cyclopentyl-1,3-dipropylxanthine prevented the CCPA-induced co-IP with RACK2. In mouse hearts, CCPA increased the co-IP of PKC-ε with RACK2 by 61%. With rat cardiomyocytes, the β-adrenergic agonist isoproterenol increased sarcomere shortening by 177%. CCPA reduced this response by 47%, an action inhibited by the PLC inhibitor U-73122 and 8-cyclopentyl-1,3-dipropylxanthine. In conclusion, A1R stimulation of the heart is associated with PLC-initiated PKC-ε translocation and association with RACK2.

scholarly journals Calcium-independent cellular damage induced by lysophosphatidylcholine in isolated rat cardiomyocytes: Comparison with the action of veratridine

1998 ◽  
Vol 76 ◽  
pp. 82
Author(s):  
Hong Ma ◽  
Hiroko Hashizume ◽  
Akiyoshi Hara ◽  
Kazuto Yazawa ◽  
Hideji Karibe ◽  
...  
Keyword(s):  
Cellular Damage ◽  
Rat Cardiomyocytes ◽  
Isolated Rat

EPA or DHA Supplementation Increases Triacylglycerol, but not Phospholipid, Levels in Isolated Rat Cardiomyocytes

Lipids ◽  
2011 ◽  
Vol 46 (7) ◽  
pp. 627-636 ◽  
Author(s):  
Valeria Righi ◽  
Mattia Di Nunzio ◽  
Francesca Danesi ◽  
Luisa Schenetti ◽  
Adele Mucci ◽  
...  
Keyword(s):  
Rat Cardiomyocytes ◽  
Isolated Rat

Comparative study of Na-blocking properties of antiarrhythmic drugs on isolated rat cardiomyocytes

1997 ◽  
Vol 123 (6) ◽  
pp. 579-581
Author(s):  
A. I. Khankoeva ◽  
A. S. Dukhanin ◽  
P. A. Galenko-Yaroshevskii
Keyword(s):  
Comparative Study ◽  
Antiarrhythmic Drugs ◽  
Rat Cardiomyocytes ◽  
Isolated Rat

scholarly journals Interaction of Metabolic and Respiratory Acidosis with α and β-adrenoceptor Stimulation in Rat Myocardium

2012 ◽  
Vol 117 (6) ◽  
pp. 1212-1222 ◽  
Author(s):  
Matthieu Biais ◽  
Romain Jouffroy ◽  
Aude Carillion ◽  
Sarah Feldman ◽  
Aude Jobart-Malfait ◽  
...  
Keyword(s):  
Metabolic Acidosis ◽  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Adenosine Monophosphate ◽  
Left Ventricular ◽  
Rat Myocardium ◽  
Adrenergic Stimulation ◽  
Rat Cardiomyocytes ◽  
Inotropic Effects ◽  
Isolated Rat

Background The effects of acute respiratory versus metabolic acidosis on the myocardium and their consequences on adrenoceptor stimulation remain poorly described. We compared the effects of metabolic and respiratory acidosis on inotropy and lusitropy in rat myocardium and their effects on the responses to α- and β-adrenoceptor stimulations. Methods The effects of acute respiratory and metabolic acidosis (pH 7.10) and their interactions with α and β-adrenoceptor stimulations were studied in isolated rat left ventricular papillary muscle (n=8 per group). Intracellular pH was measured using confocal microscopy and a pH-sensitive fluorophore in isolated rat cardiomyocytes. Data are mean percentages of baseline±SD. Results Respiratory acidosis induced more pronounced negative inotropic effects than metabolic acidosis did both in isotonic (45±3 versus 63±6%, P<0.001) and isometric (44±5 versus 64±3%, P<0.001) conditions concomitant with a greater decrease in intracellular pH (6.85±0.07 versus 7.12±0.07, P<0.001). The response to α-adrenergic stimulation was not modified by respiratory or metabolic acidosis. The inotropic response to β-adrenergic stimulation was impaired only in metabolic acidosis (137±12 versus 200±33%, P<0.001), but this effect was not observed with administration of forskolin or dibutiryl-cyclic adenosine monophosphate. This effect might be explained by a change in transmembrane pH gradient only observed with metabolic acidosis. The lusitropic response to β-adrenergic stimulation was not modified by respiratory or metabolic acidosis. Conclusion Acute metabolic and respiratory acidosis induce different myocardial effects related to different decreases in intracellular pH. Only metabolic acidosis impairs the positive inotropic effect of β-adrenergic stimulation.

Contraction-independent effects of catecholamines on glucose transport in isolated rat cardiomyocytes

1996 ◽  
Vol 270 (4) ◽  
pp. C1204-C1210 ◽  
Author(s):  
Y. Fischer ◽  
J. Thomas ◽  
G. D. Holman ◽  
H. Rose ◽  
H. Kammermeier
Keyword(s):  
Cell Surface ◽  
Glucose Transport ◽  
Basal Cells ◽  
Adrenergic Agonist ◽  
Rat Cardiomyocytes ◽  
Maximal Stimulation ◽  
Two Phases ◽  
Independent Effects ◽  
Beta Adrenergic Agonist ◽  
Isolated Rat

The effects of catecholamines on glucose transport were studied in noncontracting isolated rat cardiomyocytes. alpha-Adrenergic treatment (phenylephrine, or norepinephrine + propranolol) led to an approximately fourfold stimulation of glucose transport in basal cells (no insulin). The effect of phenylephrine was suppressed by the alpha 2-antagonist yohimbine or the beta-antagonist propranolol. The beta-adrenergic agonist isoproterenol partially counteracted the action of phenylephrine (but not that of insulin). Phenylephrine increased glucose transport in two phases with apparent half times of 3.2 and 13.0 min, respectively. Correspondingly, different EC50 values were found after 10 and 45 min on phenylephrine addition (5.0 +/- 1.9 vs. 31.6 +/- 9.6 microM, respectively). Maximal stimulation by phenylephrine was at least partially additive to that of insulin and of other stimulators of glucose transport (e.g., H2O2, vanadate, lithium). Phenylephrine significantly increased the level of cell surface glucose carriers GLUT-1 (1.54-fold) and GLUT-4 (1.78-fold), as assessed by using the specific photolabel 2-N-[4-(1-azi-2,2,2-trifluoroethyl)benzoyl]- 1,3-bis(D-mannos-4-yloxy)propyl-2-amine. In conclusion, catecholamines stimulate cardiomyocyte glucose transport through alpha 1-adrenergic receptors independently or downstream of a contraction-evoked stimulus. This effect is at least partially explained by a recruitment of glucose transporters to the cell surface. The mechanism(s) and/or signals involved differ from those triggered by insulin and insulinomimetic agents.

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