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Am J Physiol Heart Circ Physiol 279: H484-H491, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 2, H484-H491, August 2000

Arteriolar wall PO2 and nitric oxide release during sympathetic vasoconstriction in the rat intestine

Bryan A. Sauls and Matthew A. Boegehold

Department of Physiology, West Virginia University School of Medicine, Morgantown, West Virginia 26506-9229

Endothelium-derived nitric oxide (NO) attenuates arteriolar constriction in the rat small intestine during periods of increased sympathetic nerve activity. This study was undertaken to test the hypothesis that a flow-dependent fall in arteriolar wall PO2 serves as the stimulus for endothelial NO release under these conditions. Sympathetic nerve stimulation at 3-16 Hz induced frequency-dependent arteriolar constriction, with arteriolar wall O2 tension (PO2) falling from 67 ± 3 mmHg to as low as 41 ± 6 mmHg. Arteriolar responses to nerve stimulation were enhanced after inhibition of NO synthase with NG-monomethyl-L-arginine (L-NMMA). Under a high-O2 (20%) superfusate, the fall in wall PO2 was significantly attenuated, arteriolar constrictions were increased by 57 ± 9 to 66 ± 12%, and these responses were no longer sensitive to L-NMMA. The high-O2 superfusate had no effect on vascular smooth muscle responsiveness to NO (as judged by arteriolar responses to sodium nitroprusside) or on arteriolar wall oxidant activity (as determined by the reduction of tetranitroblue tetrazolium dye). These results indicate that a flow-dependent fall in arteriolar wall PO2 may serve as a stimulus for the release of endothelium-derived NO during periods of increased sympathetic nerve activity.

microvascular control mechanisms; endothelium-derived relaxing factor; sympathetic nerves; oxygen; periarteriolar O2 tension


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