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. 2016 Jul 21;594(18):5055–5077. doi: 10.1113/JP270192

Figure 3. Local increases in PO2 have no effect on arteriolar tone .

Figure 3

Data shown are modified from Jackson (1987). A, schematic diagram of a segment (1–8 mm) of an arteriole in a hamster cheek pouch from which the parenchyma has been surgically removed (aparenchymal arteriole) to obviate effects of local PO2 changes on parenchymal and other extravascular cells. A Whalen‐type recessed tip O2 microelectrode was inserted through the wall of the vessel into the lumen as shown to monitor luminal PO2. A temperature‐controlled micropipette filled with PSS equilibrated with varied PO2 (fluid‐filled micropipette) was positioned opposite the O2 microelectrode. Pressurization of the fluid‐filled micropipette ejected the O2‐equilibrated solution onto the surface of the arteriole to produce a local change in PO2 . The entire cheek pouch preparation was superfused with PSS, the PO2 of which could be varied to produce global changes in PO2 that affected both the aparenchymal arteriole and all other vessels and cell types in the cheek pouch. The diameter of the arteriole was measured by intravital video microscopy. B, results from a typical experiment in which either local increases in PO2 were produced using the fluid‐filled pipette (Local) or global increases in PO2 were produced by changing the PO2 of the entire superfusate (Global) (replotted data are from Fig. 3 in Jackson, 1987). Local increases in PO2 that effectively changed the PO2 across the wall of the arteriole had no significant effect on arteriolar diameter, whereas a global increase in PO2 produced sustained vasoconstriction. These data suggest that components of the arteriolar wall (endothelial cells, smooth muscle cells or perivascular nerves) are not the sensor cells responsible for arteriolar O2 reactivity in the hamster cheek pouch. See Jackson (1987) for details.