Effects of norepinephrine on the canine coronary sinus and atrial muscle outside of the sinus ostium were studied. In absence of electrical stimulation, norephrine caused spontaneous activity which initially arose in the atrial muscle outside of the ostium, but the pacemaker soon shifted into the coronary sinus. When the atrium was separated from the coronary sinus and norepinephrine was added, spontaneous activity occurred in the atrium but not in the sinus. Stimulation of the coronary sinus at this time triggered sustained rhythmic activity. The focus of sustained rhythmic activity in atrial tissue outside of the ostium of the coronary sinus apparently had properties different from foci found along the length of the coronary sinus. Atrial fibers outside the ostium had high resting potentials (-82 .+-. 4 mV) and action potentials with relatively rapid upstrokes (.ovrhdot.Vmax = 80 .+-. 12 V/s). They developed spontaneous diastolic depolarization when exposed to norepinephrine. Coronary sinus fibers had high resting potentials (-75 to -85 mV) and action potentials with relatively rapid upstrokes (.ovrhdot.Vmax = 129 .+-. 9 V/s). Some coronary sinus cells lost resting potential and became inexcitable when not stimulated. Norepinephrine increased resting potential in these cells, restored excitability and caused appearance of a delayed afterhyperpolarization and afterdepolarization. Afterhyperpolarizations and afterdepolarizations occurred in some cells which remained excitable after a quiescent period. Amplitude of afterdepolarizations increased when stimulus rate increased or after a premature stimulus and nondriven action potentials often arose from the peak of the afterdepolarization. Triggered sustained rhythmic activity followed. Afterdepolarizations and triggering were sometimes facilitated by a prior period of quiescence. They were inhibited by verapamil and acetylcholine.