Abstract
Chronic intermittent hypoxia (CIH) increases mean arterial pressure (MAP) and FosB/ΔFosB staining in central autonomic nuclei. To test the role of the brain RAS in CIH hypertension, rats were implanted with intracerebroventricular cannulae delivering losartan (ICVLOS: 1ug/hr) or vehicle (VEH) via mini‐osmotic pumps and telemetry devices for arterial pressure recording. A third group was given equimolar subcutaneous LOS (SCLOS) to differentiate between central and peripheral RAS effects. Rats were exposed to CIH for 7d then sacrificed for immunohistochemistry. ICV losartan had no effect on ΔMAP during CIH (VEH 5.9±0.8; ICVLOS 4.4±1.1; SCLOS 6.3±0.8 mmHg) but attenuated CIH‐induced increases in ΔMAP during the normoxic dark phase (VEH 6.7±0.8; ICVLOS 2.7±0.9; SCLOS 4.8±0.7 mmHg). Compared to VEH, ICVLOS and SCLOS attenuated FosB/ΔFosB staining in the organum vasculosum of the lamina terminalis (VEH 58±3; ICVLOS 23±6; SCLOS 37±7 cells/section). However, only ICVLOS attenuated staining in the median preoptic nucleus (VEH 31±5; ICVLOS 7±1; SCLOS 21±5 cells/section) and paraventricular (PVN) nucleus (VEH 32±7; ICVLOS 11±2; SCLOS 22± 3 cells/section). These data indicate that the central RAS contributes to the sustained, normoxic component of CIH‐induced hypertension and transcriptional activation of forebrain autonomic nuclei. Supported by P01 HL‐88052.
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