Multiple effects of extracellular ATP in cardiac tissues

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Abstract
Before its degradation to adenosine, extracellular ATP released by nerves, or by cardiac cells during ischemia, induces a positive inotropy related to stimulation of the calcium conductance by P2‐purinoceptors. This stimulation is additive with the β‐adrenergic one and seems to occur via the activation of an isoform of a Gs‐protein sensitive to cholera toxin, although with no increase in cAMP. No Phosphorylation of the CA Channel is required since the P2‐purinergic stimulation is rapidly reversible even in the presence of the poorly hydrolysable compounds ATPγS or GTPγS intracellularly. Transiently, ATP may also depolarize the cells and trigger arrhythmias by binding to a new P3‐purinoceptor type which requires Mg ions. Such a receptor induced a tyrosine phosphorylation of CI/HCO3 Exchanger, a band 3‐like protein which under such activation induces a large, transient acidosis.