EFFECTS OF GRAYANOTOXIN I ON CARDIAC NA+,K+-ADENOSINE TRIPHOSPHATASE-ACTIVITY, TRANSMEMBRANE POTENTIAL AND MYOCARDIAL CONTRACTILE-FORCE

  • 1 January 1976
    • journal article
    • research article
    • Vol. 199  (1) , 247-254
Abstract
The relationship between altered transmembrane Na movements and myocardial contractility was studied by opposing the action of the Na pump with grayanotoxin I (GTX), an agent previously shown to increase resting Na influx. GTX failed to affect Na+,K+-ATPase activity in vitro in concentrations as high as 0.1 mM. In electrically driven left atrial preparations of guinea pig hearts, 1 .mu.M GTX produced a slight depolarization and appeared to decrease the upstroke velocity of the action potential. GTX (0.1-1 .mu.M) also produced a positive inotropic effect which developed over a 20 min period. At higher concentrations, GTX produced arrhythmias. These effects of GTX were also observed in the presence of .mu.M propranolol. Positive inotropic and arrhythmic effects of GTX were reversible after washout of the drug. These effects of GTX were also reversed by tetrodotoxin, an agent which counteracted the effect of GTX on Na permeability. These data are consistent with a hypothesis that altered transmembrane Na movement affects myocardial contractility.