Figure 1.
Figure 1. Hypoxia, RBCs, and nitrite stimulate vasodilation. Nitrite-dependent vasodilation alone (▪) or in the presence of RBCs (0.3% HCT) (•) at 60 mmHg (A), 25 mmHg (B), and 15 mmHg (C) oxygen. Using a P50 value of 35 mmHg for rat RBCs and a Hill coefficient of 2.5,33,34 at 15 mmHg, 25 mmHg, and 60 mmHg oxygen, Hb saturation corresponded to 11%, 30%, and 82%, respectively, encompassing physiologic oxygen saturations. Data are mean ± SEM (n = 3). *P < .05; #P < .01 relative to the corresponding nitrite dose without RBCs. (D) EC20 (nitrite concentration that stimulated 20% dilation) values (determined from 3 independent experiments) of nitrite (▪) and nitrite + 0.3% HCT rat RBCs (□) at 15 mmHg, 25 mmHg, and 60 mmHg oxygen. *P < .01 relative to corresponding controls (n = 3).

Hypoxia, RBCs, and nitrite stimulate vasodilation. Nitrite-dependent vasodilation alone (▪) or in the presence of RBCs (0.3% HCT) (•) at 60 mmHg (A), 25 mmHg (B), and 15 mmHg (C) oxygen. Using a P50 value of 35 mmHg for rat RBCs and a Hill coefficient of 2.5,33,34  at 15 mmHg, 25 mmHg, and 60 mmHg oxygen, Hb saturation corresponded to 11%, 30%, and 82%, respectively, encompassing physiologic oxygen saturations. Data are mean ± SEM (n = 3). *P < .05; #P < .01 relative to the corresponding nitrite dose without RBCs. (D) EC20 (nitrite concentration that stimulated 20% dilation) values (determined from 3 independent experiments) of nitrite (▪) and nitrite + 0.3% HCT rat RBCs (□) at 15 mmHg, 25 mmHg, and 60 mmHg oxygen. *P < .01 relative to corresponding controls (n = 3).

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