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1 Department of Pharmacological and Physiological Science, Saint Louis University, Saint Louis, Missouri, USA
2 Department of Chemistry, Saint Louis University, Saint Louis, Missouri, USA
* To whom correspondence should be addressed. E-mail: spraguer{at}slu.edu.
Previously, it was reported that red blood cells (RBCs) are required to demonstrate participation of nitric oxide (NO) in regulation of rabbit pulmonary vascular resistance (PVR). RBCs do not synthesize NO; hence, we postulated that adenosine triphosphate (ATP), present in mM amounts in RBCs, was the mediator, which evoked NO synthesis in the vascular endothelium. First, we found that deformation of RBCs, as occurs upon passage across the pulmonary circulation with increasing flow rate, evoked increments in ATP release. Here, ATP (300 nM), administered to isolated, salt-solution perfused (PSS) rabbit lungs, decreased total and upstream (arterial) PVR, a response inhibited by L-NAME (100 µM). In lungs perfused with PSS containing RBCs, L-NAME increased total and upstream PVR. In lungs perfused with PSS containing glibenclamide-treated RBCs, which inhibits ATP release, L-NAME was without effect. Apyrase grade VII (8 U/ml), which degrades ATP to AMP, was without effect on PVR in PSS-perfused lungs. These results are consistent with the hypothesis that ATP, released from RBCs as they traverse the pulmonary circulation evokes endogenous NO synthesis.
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