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1 Department of Pharmacological and Physiological Science, Saint Louis University School of Medicine, Saint Louis, MO, USA
* To whom correspondence should be addressed. E-mail: olearcjj{at}slu.edu.
The release of ATP from erythrocytes involves a signal transduction pathway of which CFTR, PKA, adenylyl cyclase, and the heterotrimeric G proteins Gs and Gi are components. In the pulmonary circulation, ATP released from the erythrocyte stimulates NO synthesis, thereby regulating vascular resistance. We reported that NO liberated from an NO donor inhibited ATP release from erythrocytes in response to decreased oxygen tension or mechanical deformation. Here we investigated the hypothesis that NO inhibits ATP release from erythrocytes via inactivation of Gi. Washed rabbit erythrocytes were incubated in the presence or absence of the NO donor spermine NONOate (100 nM, 20 min) followed by treatment with agents that activate specific components of the signal transduction pathway promoting ATP release. Neither ATP release nor cAMP accumulation induced by either forskolin (100 µM, n = 7) or iloprost (100 nM, n = 6) was inhibited by spermine NONOate. These experiments suggest that the inhibitory action of NO is not the result of inactivation of adenylyl cyclase or Gs, respectively. However, spermine NONOate completely inhibited ATP release in response to mastoparan (10 µm, P<0.05, n = 5), a specific activator of Gi. Spermine (100 nM, 20 min), the polyamine remaining after liberation of NO from spermine NONOate, had no affect on mastoparan-induced ATP release (n = 4). These results support the hypothesis that NO inhibits ATP release from erythrocytes via inactivation of the heterotrimeric G protein Gi.
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