Exposure to the frog heart to single, millisecond length pulses of ultrasound has been shown to cause effects by two qualitatively different physical mechanisms. One of these effects has also been observed in mice. When the pulse is delivered during systole, it can cause a reduction in the developed aortic pressure. Evidence suggests that this arises from an action of radiation force on the heart tissues. The effect can be produced with an acoustic reflector over the heart. This maximizes the radiation force delivered to the heart, but eliminates direct interaction of the ultrasound with the heart tissue, thus experimentally eliminated heating and cavitation as mechanisms of action. When the pulse is delivered during diastole, it can produce a premature ventricular contraction. No premature ventricular contractions were observed with the acoustic reflector over the heart. The mechanism is nonthermal. Available evidence does not preclude cavitation as the primary physical mechanism responsible for premature ventricular contractions.