External ATP-induced changes in [Ca2+]i and membrane currents in mammalian atrial myocytes.

Fura-2 fluorescent digital-imaging microscopy and whole cell patch-clamp recordings were used to study the effects of externally applied ATP on atrial myocytes isolated from rabbit and guinea pig hearts. Application of 100 microM ATP elicited a transient increase in intracellular calcium concentration ([Ca2+]i), which was not suppressed by theophylline, whereas adenosine and ADP failed to evoke the response. The Ca2+ transients were suppressed by the application of Co2+, Ni2+, or verapamil and by the removal of extracellular Ca2+, indicating that the inflow of external Ca2+ is necessary to evoke the response. The Ca2+ transient was suppressed also by ryanodine, suggesting that the mobilization of intracellular Ca2+ is another important factor. In the whole cell recordings, ATP induced a transient depolarization of the membrane potential due to the activation of a rapidly desensitizing inward current which persisted in the presence of Co2+, Ni2+, verapamil, or ryanodine. These results indicate that in mammalian atrial myocytes, ATP evoked transient increase in [Ca2+]i via P2-receptor, through the release of internally stored Ca2+ associated with the inflow of external Ca2+. This response seemed to be triggered mainly by the influx of Ca2+ through L-type Ca2+ channel activated by membrane depolarization, which was caused by the ATP-induced inward current.