We investigated effects of extracellular ATP on intracellular chloride activities ([Cl
-]
i) and possible contribution of the Cl
--HCO
3- exchange to this increase in [Cl
-]
i in isolated guinea pig ventricular muscles. The [Cl
-]
i and intracellular pH (pH
i) were recorded in quiescent ventricular muscles using double-barreled ion-selective microelectrode techniques. MgATP at a concentration higher than 0.1mM, induced an increase in [Cl
-]
i, and this increase in [Cl
-]
i was dependent on the concentration of ATP but not on the concentration of magnesium ions present in the perfusion solution. NaADP, but not NaAMP, at a concentration of 0.5mM induced a similar increase in [Cl
-]
i as that induced by MgATP. However, the NaADP-induced increase in [Cl
-]
i was transient and gradually returned to the control level even though NaADP was continuously present. Furthermore, ATP also triggered a transient acidification of pH
i, and both increases in [Cl
-]
i and intracellular H
+ induced by ATP were prevented when preparations were pretreated with stilbene derivatives, SITS and DIDS, or perfused with a Cl
--free solution. Our findings showed that the increased extracellular ATP concentrations might trigger an increase in [Cl
-]
i in ventricular muscles. In light of previous studies showing that cardiac ischemia induced increases in extracellular nucleotide concentrations and [Cl
-]
i in ventricular muscles, we propose that ischemia-induced accumulation of ATP concentration in the extracellular space may be an important factor to trigger increment of [Cl
-]
i during ischemic conditions.
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