Figure 6. Keratinocyte deletion of NOS2 affects cardiovascular acclimation to hypoxia.

Mice were individually housed for 14 hr in normoxia before being exposed to hypoxia (10%) at the light-dark interphase for 48 hr. Mice then recovered for a further 24 hr in normoxia. (A) Skin temperature acclimation in littermate (black line, n = 7) and K14cre-NOS2 (red line n = 5). Data shown as mean degree’s Celsius (shaded area depicts dark cycle). (B) Deletion efficiency of NOS2 in K14cre+ mice was calculated by Taq-man PCR. (C) Acute and (D) chronic analysis of systolic and diastolic blood pressure in littermate (black-line and grey-line n = 8) and K14cre-NOS2 (dark red line and light red line n = 5) data shown as mean (mm/Hg). Lower line graph shows blood pressure deviation for both systolic (light red) and diastolic (dark red) BP. (E) Acute and (F) chronic analysis of heart rate in littermate (black line n = 6) and K14cre-NOS2 (red line n = 5). Data shown as mean beats per minute. Lower line graph shows chronic heart rate deviation of K14cre-NOS2 from littermate. (G and H) RT-qPCR analysis of whole skin samples from K14cre-NOS2 (n = 6) and littermate mice (n = 6) following 6 hr hypoxia (10% O₂) exposure. (G) Epidermal NOS2 deletion stimulates enhanced expression of NOS1 and NOS3. (H) Skin VEGF expression is not effect by NOS2. (I) Analysis of physical activity in littermate (black line n = 6) and K14cre-NOS2 (red line n = 7) during acclimation to chronic hypoxia. Data shown as mean activity meters/hour.