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

Endothelium-derived nitric oxide (NO) attenuates arteriolar constriction in the rat small intestine during periods of increased sympathetic nerve acti vity. This study was undertaken to test the hypothesis that a flow-dependen t fall in arteriolar wall PO2 serves as the stimulus for endothelial NO rel ease under these conditions. Sympathetic nerve stimulation at 3-16 Hz induc ed frequency-dependent arteriolar constriction, with arteriolar wall O-2 te nsion (PO2) falling from 67 +/- 3 mmHg to as low as 41 +/- 6 mmHg. Arteriol ar responses to nerve stimulation were enhanced after inhibition of NO synt hase with N-G-monomethyl-L-arginine (L-NMMA). Under a high-O-2 (20%) superf usate, the fall in wall PO2 was significantly attenuated, arteriolar constr ictions were increased by 57 +/- 9 to 666 12%, and these responses were no longer sensitive to L-NMMA. The high-O-2 superfusate had no effect on vascu lar smooth muscle responsiveness to NO (as judged by arteriolar responses t o sodium nitroprusside) or on arteriolar wall oxidant activity (as determin ed by the reduction of tetranitroblue tetrazolium dye). These results indic ate that a flow-dependent fall in arteriolar wall PO2 may serve as a stimul us for the release of endothelium-derived NO during periods of increased sy mpathetic nerve activity.