Figure 5.

Chronic myocardial hypoxia in anemic animals persistently reduces NHE1 activity. (A) Intrinsic buffering capacity in myocytes from control (n = 20 cells, 3 mice) and anemic mice (n = 23 cells, 3 mice). No significant difference (two-way ANOVA). (B) Resting pH_i under Hepes-buffering regime (n = 124 and 121 cells from 3 anemic and 3 control mice, respectively); t-test, P < 0.01. (C) Time course of pH_i recovery following an ammonium prepulse. Average of 46 myocytes from three control hearts and 36 myocytes from three anemic hearts. Error bars not shown for clarity. (D) NHE1 generated flux in myocytes from control (n = 46 cells from 3 mice) and anemic (n = 36 cells from 3 mice) animals, showing significant decrease in the latter; two-way ANOVA: significant (P < 0.01) effect of anemic intervention. (E) Levels of transcripts for the gene coding NHE1, Slc9a1, is not different between anemic and control hearts. Whole heart tissue mRNA from 9 mice per group. Used as a control, Na⁺/K⁺ pump genes Atp1a1 and Atp1a2 are unchanged. (F) Apparent H⁺ diffusion coefficient is significantly increased in myocytes from anemic mice (n = 12 from 3 mice) relative to control myocytes (n = 12 from 3 mice); t-test, P < 0.01.