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Reduced perivascular PO₂ increases nitric oxide release from endothelial cells

Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis, Indiana 46202

Submitted 29 August 2002 ; accepted in final form 30 January 2003

Many studies have suggested that endothelial cells can act as "oxygen sensors" to large reductions in oxygen availability by increasing nitric oxide (NO) production. This study determined whether small reductions in oxygen availability enhanced NO production from in vivo intestinal arterioles, venules, and parenchymal cells. In vivo measurements of perivascular NO concentration ([NO]) were made with NO-sensitive microelectrodes during normoxic and reduced oxygen availability. During normoxia, intestinal first-order arteriolar [NO] was 397 ± 26 nM (n = 5), paired venular [NO] was 298 ± 34 nM (n = 5), and parenchymal cell [NO] was 138 ± 36 nM (n = 3). During reduced oxygen availability, arteriolar and venular [NO] significantly increased to 695 ± 79 nM (n = 5) and 534 ± 66 nM (n = 5), respectively, whereas parenchymal [NO] remained unchanged at 144 ± 34 nM (n = 4). During reduced oxygenation, arteriolar and venular diameters increased by 15 ± 3% and 14 ± 5%, respectively: N^G-nitro-L-arginine methyl ester strongly suppressed the dilation to lower periarteriolar PO₂. Micropipette injection of a CO₂ embolus into arterioles significantly attenuated arteriolar dilation and suppressed NO release in response to reduced oxygen availability. These results indicated that in rat intestine, reduced oxygen availability increased both arteriolar and venular NO and that the main site of NO release under these conditions was from endothelial cells.

embolization; partial pressure of oxygen

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