Thirty-six isolated frog ventricles were attached to an inflow cannula with stopcocks that could permit direct systolic ejection back into the reservoir, return flow back to the reservoir by another route through a valve, or isochorie contractions. The heart, enclosed in a container with a “U” tube outlet, produced pressure changes (extra-cardiac) which could be used in determining the in-flow rate and transmural pressures. The rate of change of the transmural pressure was calculated for the frog ventricle during early diastole. This value was taken as a measurement of the rate of relaxation. The effects of epinephrine (.02 μg./ml.) were studied. At low filling pressures without valves (and therefore with outflow pressure equal to inflow pressure), epinephrine slows the rate of relaxation, although other inotropic effects, such as an increase in stroke volumes, are present. If, however, the heart contracts against a high outflow pressure or resistance the rate of relaxation is increased by epinephrine. The slowing of relaxation in the former case is a result of filling commencing before relaxation is complete. In the isochoric heart, epinephrine does not change the time of positive tension, but does accelerate the relaxation after contraction.