Fig. 8.

Carvedilol (1 µM) suppresses spontaneous Ca²⁺ waves. Ca²⁺ wave frequency was quantified during a period of rest (20 s) after pacing (1 Hz) in elevated extracellular Ca²⁺ concentration ([Ca²⁺]_o; 7 mM). A; whole cell [Ca²⁺]_i profiles and confocal line scan images in control (top) and carvedilol-treated (bottom) atrial myocytes (n = 10). Black circles indicate stimulus during electrical pacing. B: average carvedilol effect on Ca²⁺ wave frequency. *P < 0.004 (paired t-test). C: average wave latency [Δt between last electrically elicited Ca²⁺-transient (CaT) and first Ca²⁺ wave] in control (Ctrl) and carvedilol-treated atrial myocytes (unpaired t-test). D: average Ca²⁺ wave velocity in control and carvedilol-treated atrial myocytes (unpaired t-test). E: carvedilol effect on sarcoplasmic reticulum (SR) Ca²⁺ load. SR load was quantified as the amplitude of a CaT elicited by rapid superfusion with caffeine (10 mM) in control (top) and in the presence of carvedilol (1 µM; bottom). Whole cell intracellular Ca²⁺ concentration ([Ca²⁺]_i) profiles and corresponding line scan images are shown. F: summary of CaT amplitudes in response to 10 mM caffeine (n = 11; paired t-test). NS, not significant.