AJP - Cell Physiology, Vol 260, Issue 6 C1182-C1190, Copyright © 1991 by American Physiological Society

ARTICLES

Extracellular ATP activates coordinated Na+, Pi, and Ca2+ transport in cardiac myocytes

M. B. De Young and A. Scarpa
Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106.

Activation of an ATP receptor has previously been shown to induce cytosolic [Ca2+] transients in rat ventricular myocytes. A slower but larger [Ca2+] increase which can cause cell hypercontraction follows the transient when extracellular Pi is increased. This second phase of the [Ca2+] response is stimulated by ATP or adenosine 5'-(gamma-thio)triphosphate in a medium containing 11.2 mM Pi, but not by high concentrations of 2-methylthio-ATP, which stimulate only the initial [Ca2+] transient. Replacing medium Na+ with N-methyl-D-glucamine suppresses this Pi-dependent [Ca2+] increase following ATP addition, suggesting a causal relationship between Na+ transport and Ca2+ influx. Blocking voltage-sensitive Na+ channels, Na(+)-H+ exchange, or Na(+)-K(+)-Cl- cotransport did not reduce ATP-induced cell hypercontraction in 11.2 mM Pi medium, suggesting that these transporters are not involved. ATP stimulation of Na(+)-Pi cotransport was investigated with isotopic methods. The results were consistent with the hypothesis that extracellular ATP stimulates Na(+)-Pi cotransport, which activates Na(+)-Ca2+ exchange. A novel Pi-dependent ATP receptor-effector system has been demonstrated in cardiac cells, and it may have significant effects on cellular transport, contractility, and bioenergetics.

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