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Heterotrimeric G protein G_i is involved in a signal transduction pathway for ATP release from erythrocytes

Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, St. Louis, Missouri 63104

Submitted 18 July 2003 ; accepted in final form 4 November 2003

Erythrocytes are reported to release ATP in response to mechanical deformation and decreased oxygen tension. Previously we proposed that receptor-mediated activation of the heterotrimeric G protein G_s resulted in ATP release from erythrocytes. Here we investigate the hypothesis that activation of heterotrimeric G proteins of the G_i subtype are also involved in a signal transduction pathway for ATP release from rabbit erythrocytes. Heterotrimeric G proteins G_i1, G_i2, and G_i3 but not G_o were identified in rabbit and human erythrocyte membranes. Pretreatment of rabbit erythrocytes with pertussis toxin (100 ng/ml, 2 h), which uncouples G_i/o from their effector proteins, inhibited deformation-induced ATP release. Incubation of rabbit and human erythrocytes with mastoparan (Mas, 10 µM) or Mas-7 (1 µM), which are compounds that directly activate G_i proteins, resulted in ATP release. However, rabbit erythrocytes did not release ATP when incubated with Mas-17 (10 µM), which is an inactive Mas analog. In separate experiments, Mas (10 µM) but not Mas-17 (10 µM) increased intracellular concentrations of cAMP when incubated with rabbit erythrocytes. Importantly, Mas-induced ATP release from rabbit erythrocytes was inhibited after treatment with pertussis toxin (100 ng/ml, 2 h). These data are consistent with the hypothesis that the heterotrimeric G protein G_i is a component of a signal transduction pathway for ATP release from erythrocytes.

pulmonary circulation; red blood cells; mechanical deformation; adenine nucleotides

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