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. 2020 Sep 14;9:e59499. doi: 10.7554/eLife.59499

Figure 2. CO2 constricts pial vessels in the RTN region by a P2Y2 receptor-dependent mechanism to increase respiratory behavior in anesthetized mice.

Figure 2.

(A) Images of RTN pial vessels and corresponding traces of vessel diameter (N = 6 mice/condition) show that exposure to 9–10% CO2 decreased vessel diameter under control conditions (saline) but not when P2Y2 receptors were blocked with AR-C118925 (1 mM). (B) Images of RTN pial vessels and corresponding traces vessel diameter show that application of a P2Y2 receptor agonist (PSB1114; 100 µM) caused a reversible constriction. (C-D) Traces of external intercostal EMG (IntEMG) and end expiratory CO2 (etCO2) show that blocking CO2/H+-induced vasoconstriction by ventral surface application of AR-C118925 minimally affected respiratory activity at low etCO2 levels but blunted the ventilatory response to 9–10% CO2 (C). Conversely, at a constant etCO2 of 5% the application of PSB1114 to mimic CO2/H+ constriction increased respiratory output (D). (E-J) Summary data show (N = 6 mice/condition) effects RTN application of saline, AR-C118925 or PSB1114 on intercostal EMG amplitude (E, H), frequency (F, I) and mean arterial pressure (MAP; G, J). *, Different (RM-ANOVA followed by Bonferroni multiple-comparison test; *, p<0.05). scale bar = 200 μm.