Mechanisms of Automaticity in Subsidiary Pacemakers From Cat Right Atrium

Intracellular recordings were made from eustachian ridge of cat right atrium to determine mechanisms responsible for subsidiary pacemaker automaticity. Pacemaker action potentials exhibited two phases of diastolic depolarization: an initial steeper slope (D,) followed by a more gradual slope (D2). Cesium (1 mM) decreased D, (—45.6%) to a significantly greater extent than D2 (-33.6%) and increased spontaneous cycle length (SCL) (+37.7%). Tetrodotoxin (10" ' M) had no effect on maximum rate of rise of upstroke, although it increased SCL (+23.9%). Verapamil (0.4-1.0 fiM) progressively increased SCL by decreasing late diastolic slope, resulting in oscillatory potentials and eventual quiescence. Both norepinephrine (2x 10"9 M) and Bay K 8644 (10~7 M) elicited a significantly greater increase in D2 than in D,, resulting in a decrease in SCL. Ryanodine (10~6 M) caused a small but significant initial decrease (—3.7%) followed by a progressive increase in SCL (+172%). Ryanodine decreased D2 without changing D,, increased maximum rate of rise and overshoot potential, and abolished tension. In the presence of ryanodine, Bay K 8644 progressively increased D, amplitude, resulting in a cyclic pattern of dysrhythmic activity. In the presence of ryanodine, cesium significantly decreased D, (-39.3%), shifted the late diastolic potential more negative, and increased SCL (+25.7%)