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Rat atria either beating spontaneously or electrically driven were were perfused in vitro at 30 degrees C. When the preparations were exposed to harmaline 8.3 x 10(-5) or 16.6 x 10(-5) M the atrial rate showed down and the following changes in membrane potentials were observed: (1) a transient increase in the amplitude of the action potential (AAP), in the absence of any change in the magnitude of the resting potential (RP), followed by a progressive decrease of AaP; (2) a progressive decline of the slope of the fast ascending phase of the action potential, which was initially independent of any change in the magnitude of the rp; (3) a progressive increase of the duration of the action potential; (4) a fall in the magnitude of the resting potential. The conclusions proposed are that harmaline: (1) stimulates the slow current responsible for the last part of the upstroke and the beginning of the repolarization; (2) inhibits the sodium current responsible for the fast component of the upstroke; (3) slows doen the processes responsible for the repolarization; (4) inhibits the (Na+-K+) activated membrane ATPase.

In rat isolated right atria, beating spontaneously at 30 degrees C, harmaline 8.3 times 10-5 M slowed atrial rate and enhanced force of contraction. The velocity of development of tension (dT/dt) increased and time to peak tension was lengthened. Electrical drive of otherwise quiescent left atria showed that (1) within the range of change of rate induced by harmaline the reduction of frequency of stimulation increased dT/dt and peak tension developed, and (2) at a constant rate of stimulation harmaline produced a prolongation of time to peak tension and an enhancement of peak tension. We concluded that two mechanisms are responsible for the inotropic action of harmaline on rat atrium: (1) an increase in dT/dt due to the lengthening of the interval between beats; (2) a direct action of harmaline on the processes responsible for atrial contraction, which determines a lengthening of time to peak tension.