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Am J Physiol Heart Circ Physiol 285: H693-H700, 2003. First published April 10, 2003; doi:10.1152/ajpheart.01026.2002
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Extracellular ATP signaling in the rabbit lung: erythrocytes as determinants of vascular resistance

Randy S. Sprague,1 Jeffrey J. Olearczyk,1 Dana M. Spence,2 Alan H. Stephenson,1 Robert W. Sprung,2 and Andrew J. Lonigro1

Departments of 1Pharmacological and Physiological Science and 2Chemistry, School of Medicine, Saint Louis University, St. Louis, Missouri 63104

Submitted 6 December 2002 ; accepted in final form 8 April 2003

Previously, it was reported that red blood cells (RBCs) are required to demonstrate participation of nitric oxide (NO) in the regulation of rabbit pulmonary vascular resistance (PVR). RBCs do not synthesize NO; hence, we postulated that ATP, present in millimolar amounts in RBCs, was the mediator, which evoked NO synthesis in the vascular endothelium. First, we found that deformation of RBCs, as occurs on 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 NG-nitro-L-arginine methyl ester (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.

adenosine-5' triphosphate; red blood cell


Address for reprint requests and other correspondence: Randy S. Sprague, Dept. of Pharmacological and Physiological Science, School of Medicine, Saint Louis Univ., 1402 South Grand Blvd., St. Louis, MO 63104 (E-mail: spraguer{at}slu.edu).




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