In previous work we induced intermittent hypoxia (IH) for 4 hours each day for 8 weeks (10% O2 normobaric chamber), which simulated the degree and duration of hypoxia in severe human sleep apnoea. A second group of rats was continuously exposed to the reduced O2 tension in the chamber (CH).These groups were compared with a normoxic group (N). GLUT 1 (Glucose transporter 1, an endothelial cell marker, indicating viable vascularity) immunostaining was significantly (P< 0.02) increased in 5 brain areas, to a greater extent in CH rather than in the IH group. Under thiopentone anaesthesia (100mg/kg ip), pulmonary artery pressure (Ppa) was measured with a curved catheter inserted through the external jugular vein to the right atrium) and systemic pressure was measured in a femoral artery. After a lethal dose of thiopentone, the heart and lungs were removed and the brain perfused through the aorta with buffered formalin at 120 mmHg. Ppa was raised and there was right ventricular hypertrophy (RVH), again to a greater extent in CH compared to the IH group. There was wall thickening in small lung arterioles (Kalaria et al., 2004). Systemic hypertension is often associated with sleep apnoea and may be causally related. Thus we have repeated the above regimes in rat groups (n=4-6/group) with systemic hypertension induced by NOS blockade with L-NAME in drinking water (NLN, IHLN and CHLN). GLUT 1 immunostaining was assessed, in each group, and expressed as mean % staining per area (±SD; Student's t test, significance p ≤ 0.05). Results from 4 brain areas were: Cortex A, NLN 2.481(±1.15), IHLN 2.522 (±0.96), CHLN 3.001 (±1.31) CHLN vs NLN P<0.05). Cortex B, NLN 3.383(±1.05), IHLN 3.00 (±0.86), CHLN 4.966 (±1.68) CHLN vs NLN P<0.01). Putamen, NLN 2.657 (±0.86), IHLN 3.099 (±1.00), CHLN 4.853(±1.16) CHLN vs NLN P<0.01). Hippocampus, NLN 2.101 (±0.96), IHLN 2.088(±0.85, CHLN 2.801 (±1.17) CHLN vs NLN P<0.01). Thus GLUT 1 immunostaining was significantly greater in 4 brain regions in the CHLN group than the NLN group, but was not greater in IHLN groups than the NLN groups. GLUT 1 analysis suggests that systemic hypertension, caused by L-NAME inhibits cerebral angiogenesis in intermittent hypoxia. Ppa was not raised in IHLN, nor was there RVH. There was wall thickening in small lung vessels. Thus vascular thickening is likely to be due to hypoxia rather than pressure. Cardiopulmonary changes were also inhibited in the presence of systemic hypertension.