Adenosine linking reduced O2 to arteriolar NO release in intestine is not formed from extracellular ATP

Bryan A. Sauls, Matthew A. Boegehold
2001 American Journal of Physiology. Heart and Circulatory Physiology  
Adenosine linking reduced O2 to arteriolar NO release in intestine is not formed from extracellular ATP. Am J Physiol Heart Circ Physiol 281: H1193-H1200, 2001.-We have previously reported that adenosine formed in response to reduced arteriolar and/or tissue PO2 preserves endothelial nitric oxide (NO) synthesis during sympathetic vasoconstriction in the rat intestine. To more precisely identify the site and mechanism of adenosine formation under these conditions, we tested the hypothesis that
more » ... e hypothesis that ATP released in response to reduced O2 levels serves as a source of adenosine. Direct application of ATP to the wall of first-order arterioles elicited dose-dependent dilations of 15-33% above resting diameter that were reduced by 71-80% by the 5Ј-ectonucleotidase inhibitor ␣,␤-methyleneadenosine 5Ј-diphosphate (AOPCP, 4.5 ϫ 10 Ϫ5 M) and completely abolished by N G -monomethyl-L-arginine (L-NMMA, 10 Ϫ4 M). Under control conditions, sympathetic nerve stimulation at 3 and 8 Hz induced arteriolar constrictions of 11 Ϯ 1 and 19 Ϯ 1 m, respectively. These responses were enhanced by 58-69% in the presence of L-NMMA or when local PO2 was maintained at resting levels. However, in the presence of AOPCP, the enhancing effects of L-NMMA and the high O2 superfusate on sympathetic constriction were preserved. These results suggest that, although exogenously applied ATP can stimulate arteriolar NO release in the intestine largely through its sequential extracellular hydrolysis to adenosine, this process does not contribute to adenosine formation and sustained NO release during sympathetic constriction in this vascular bed.
doi:10.1152/ajpheart.2001.281.3.h1193 pmid:11514287 fatcat:337pxvqzwjcvhiiud4ubugnvu4