Sodium pump inhibition by sulfhydryl inhibitors and myocardial contractility

1978 ◽  
Vol 302 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Kyosuke Temma ◽  
Tai Akera ◽  
David D. Ku ◽  
Theodore M. Brody
Keyword(s):  
Myocardial Contractility ◽  
Sodium Pump ◽  
Sodium Pump Inhibition

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

Sensitive assay for sodium pump inhibition

1994 ◽  
Vol 40 (8) ◽  
pp. 1595-1596 ◽  
Author(s):  
Q F Tao ◽  
P A Soszynski ◽  
N K Hollenberg ◽  
S W Graves
Keyword(s):  
Sodium Pump ◽  
Sensitive Assay ◽  
Sodium Pump Inhibition

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

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.

Interactions of diphenylhydantoin and cardiac glycosides on atrial potassium

1976 ◽  
Vol 230 (4) ◽  
pp. 965-969 ◽  
Author(s):  
CK Loh ◽  
AM Katz ◽  
Peirce EC
Keyword(s):  
Action Potential ◽  
Therapeutic Effect ◽  
Action Potential Duration ◽  
Cardiac Glycosides ◽  
Sodium Pump ◽  
Atrial Myocardium ◽  
Digitalis Toxicity ◽  
Tension Response ◽  
Sodium Pump Inhibition ◽  
Total Tissue

Effects of diphenylhydantoin (DPH) on amphibian atrial myocardium K were investigated using a method which permits both total tissue K and tension response to be monitored continuously. In normal (nondigitalized) preparations, DPH caused a decrease in average K efflux, a net gain of tissue K, and negativeinotropy at low perfusate K concentrations. However, the DPH-induced gain of tissue K was abolished at high perfusate K concentrations while marked negative inotropy was still observed. It is concluded that a gain of tissue K is not the cause of DPH-induced negative inotropy. When digitalis-induced inotropy was associated with tissue K loss, DPH reversed tissue K loss and positive inotropy and caused a decrease in average K efflux. In the presence of toxic effects of digitalis, DPH reversed the K loss and the contracture, but the loss of developed tension was not reversed by DPH. Transmembrane resting potentials and action potential duration were reduced by digitalis and were returned to or above control levels in the presence of DPH. The present findings are consistent with the hypothesis that the therapeutic effect of DPH in digitalis toxicity is brought about by an inhibition of K efflux. This would tend to minimize the loss of tissue K which results from sodium pump inhibition.

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