Effects of rubidium on contractility and sodium pump activity in guinea-pig ventricle

Inhibition of the Na+-K+ active transport system has been postulated to be one mechanism through which myocardial contractility is increased. Rubidium is one substance which has been shown to increase the contractility of guinea-pig atria and inhibit the activity of the isolated Na+,K+-adenosine triphosphatase of guinea-pig ventricle. A reexamination of these results confirmed the positive inotropic effect of rubidium on guinea-pig atria and demonstrated that this effect on contractility is accompanied by a decrease in both resting potential and action potential duration. However, it was also found that rubidium produced a transient negative inotropic effect in guinea-pig ventricle. The latter response was closely paralleled by a transient shortening of action potential duration. A concentration of rubidium maximally effective in decreasing contractility (2.0 mM) had no effect on the slow response action potential or contraction. RbCl (0.1 mM) had no effect on cyclic adenosine 3':5'-monophosphate levels of the ventricle or atrium. RbCl did inhibit active transport in the ventricle, as evidenced by a significant reduction in the electrogenic contribution on the active transport system to the maximal diastolic membrane potential during high-frequency drive. These results demonstrate that RbCl has different effects on the contractility of atrial and ventricular muscle. They also suggest that inhibition of the sodium pump is not necessarily accompanied by an increased force of myocardial contraction.