scholarly journals Relation of sodium pump inhibition to positive inotropy at low concentrations of ouabain in rat heart muscle.

1985 ◽  
Vol 360 (1) ◽  
pp. 149-160 ◽  
Author(s):  
I Grupp ◽  
W B Im ◽  
C O Lee ◽  
S W Lee ◽  
M S Pecker ◽  
...  
Keyword(s):  
Heart Muscle ◽  
Rat Heart ◽  
Sodium Pump ◽  
Positive Inotropy ◽  
Low Concentrations ◽  
Sodium Pump Inhibition

Carnitine effects on palmitate-1-C14 conversion to CO2 and glycerides by various tissues

1964 ◽  
Vol 206 (6) ◽  
pp. 1217-1222 ◽  
Author(s):  
Irving B. Fritz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Rat Heart ◽  
Liver Microsomes ◽  
Tissue Homogenate ◽  
Acid Oxidation ◽  
Acid Oxidase ◽  
Palmitate Oxidation ◽  
Glyceride Synthesis ◽  
Low Concentrations

Carnitine increased oxidation of palmitate-1-C14 by rat heart and liver preparations, but decreased palmitate incorporation into glycerides. To determine which of the effects was derivative and which was primary, experiments were repeated using tissues whose rates of fatty acid oxidation had been depressed by Amytal poisoning. Under these conditions, carnitine inhibition of fatty acid conversion to glycerides was abolished. Similarly, low concentrations of carnitine were found to enhance palmitate oxidation without influencing palmitate esterification. Isolated liver microsomes which synthesized glycerides without oxidizing fatty acids showed no response to carnitine under all conditions tried. The inability of carnitine to alter glyceride formation in experiments described may signify that acyl-CoA generation from CoA and acylcarnitine is specifically directed toward the fatty acid oxidase system rather than to glyceride synthesis. It was also shown that, under conditions optimal for demonstration of carnitine augmentation of fatty acid oxidation by rat heart preparations, carnitine increased palmitate oxidation by a variety of other tissue homogenate preparations.

Metabolic fate of rat heart endothelial lipoprotein lipase

1988 ◽  
Vol 255 (3) ◽  
pp. E247-E254 ◽  
Author(s):  
T. Chajek-Shaul ◽  
G. Bengtsson-Olivecrona ◽  
J. Peterson ◽  
T. Olivecrona
Keyword(s):  
Lipoprotein Lipase ◽  
Lipase Activity ◽  
Rat Heart ◽  
Metabolic Fate ◽  
Low Concentrations ◽  
Rat Hearts ◽  
Catalytically Active ◽  
Isolated Rat

When isolated rat hearts were perfused with medium containing 125I-labeled bovine lipoprotein lipase (LPL), they bound both lipase activity and radioactivity. More than 80% of the bound lipase could be rapidly released by heparin. Low concentrations of bovine LPL displaced 50-60% of the endogeneous, endothelial-bound LPL. Higher concentrations caused additional binding. Both binding and exchange were rapid processes. The hearts continuously released endogenous LPL into the medium. An antiserum that inhibited bovine but not rat LPL was used to differentiate endogeneous and exogeneous LPL activity. When the pool of endothelial LPL was labeled with bovine 125I-labeled LPL and then chased with unlabeled bovine LPL, approximately 50% of the labeled lipase was rapidly displaced. During chase perfusion with medium only, catalytically active bovine LPL appeared in the perfusate. The rate of release was similar to that observed for endogeneous LPL activity and amounted to 10-13% of the heparin-releasable fraction in the first 5 min of perfusion. There was little or no degradation of bovine 125I-labeled LPL to fragments or acid-soluble products. These results indicate that endothelial LPL is accessible for exchange with exogeneous LPL and that detachment rather than degradation may be the pathway for catabolism of endothelial LPL.

Effects of endogenous calcium transport inhibitor from heart muscle on the active calcium uptake and passive calcium release properties of sarcoplasmic reticulum

1989 ◽  
Vol 67 (9) ◽  
pp. 999-1006 ◽  
Author(s):  
Njanoor Narayanan ◽  
Philip Bedard ◽  
Trilochan S. Waraich
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Heart Muscle ◽  
Calcium Release ◽  
Membrane Vesicles ◽  
Transport Inhibitor ◽  
Low Concentrations ◽  
Active Calcium ◽  
High Concentrations ◽  
Stimulation Of

In the present study, the effects of the cytosolic Ca2+ transport inhibitor on ATP-dependent Ca2+ uptake by, and unidirectional passive Ca2+ release from, sarcoplassmic reticulum enriched membrane vesicles were examined in parallel experiments to determine whether inhibitor-mediated enhancement in Ca2+ efflux contributes to inhibition of net Ca2+ uptake. When assays were performed at pH 6.8 in the presence of oxalate, low concentrations (<100 μg/mL) of the inhibitor caused substantial inhibition of Ca2+ uptake by SR (28–50%). At this pH, low concentrations of the inhibitor did not cause enhancement of passive Ca2+ release from actively Ca2+-loaded sarcoplasmic reticulum. Under these conditions, high concentrations (>100 μg/mL) of the inhibitor caused stimulation of passive Ca2+ release but to a much lesser extent when compared with the extent of inhibition of active Ca2+ uptake (i.e., twofold greater inhibition of Ca2+ uptake than stimulation of Ca2+ release). When Ca2+ uptake and release assays were carried out at pH 7.4, the Ca2+ release promoting action of the inhibitor became more pronounced, such that the magnitude of enhancement in Ca2+ release at varying concentrations of the inhibitor (20–200 μg/mL) was not markedly different from the magnitude of inhibition of Ca2+ uptake. In the absence of oxalate in the assay medium, inhibition of Ca2+ uptake was observed at alkaline but not acidic pH. These findings imply that the inhibition of Ca2+ uptake observed at pH 6.8 is mainly due to decrease in the rate of active Ca2+ transport into the membrane vesicles rather than stimulation of passive Ca2+ efflux; at alkaline pH (pH 7.4), enhanced Ca2+ efflux contributes substantially, if not exclusively, to the decrease in Ca2+ uptake observed in the presence of the inhibitor. It is suggested that if the cytosolic inhibitor has actions similar to those observed in vitro in intact cardiac muscle, acid–base status of the intracellular fluid would be a major factor influencing the nature of its effects (inhibition of Ca2+ uptake or stimulation of Ca2+ release) on transmembrane Ca2+ fluxes across the sarcoplasmic reticulum.Key words: sarcoplasmic reticulum, Ca2+ uptake, Ca2+ release, endogenous inhibitor, heart muscle.

Effects of sodium pump inhibition on the relaxation induced by synthetic Atrial Natriuretic Factor (ANF) and sodium nitroprusside

1985 ◽  
Vol 10 ◽  
pp. 110-112
Author(s):  
Michel Auguet ◽  
Sylvie Delaflotte ◽  
Ricardo Garay ◽  
Marc Cantin ◽  
François Clostre ◽  
...  
Keyword(s):  
Sodium Nitroprusside ◽  
Atrial Natriuretic Factor ◽  
Sodium Pump ◽  
Natriuretic Factor ◽  
Sodium Pump Inhibition ◽  
Atrial Natriuretic

Reducing the Late Sodium Current Improves Cardiac Function during Sodium Pump Inhibition by Ouabain

2011 ◽  
Vol 337 (2) ◽  
pp. 513-523 ◽  
Author(s):  
Kirsten Hoyer ◽  
Yejia Song ◽  
Desuo Wang ◽  
Dillon Phan ◽  
James Balschi ◽  
...  
Keyword(s):  
Cardiac Function ◽  
Sodium Pump ◽  
Sodium Current ◽  
Late Sodium Current ◽  
Sodium Pump Inhibition
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