Chronic intermittent hypoxia (CIH), a preclinical model of hypoxemia associated with sleep apnea, causes hypertension associated with increased sympathetic activity linked to arterial chemoreflex and renin-angiotensin system activation. In some models of CIH, ovarian hormones have a protective effect against the change in blood pressure. We tested the effects of CIH and ovariectomy (OVX) on blood pressure and ΔFosB expression in female Sprague-Dawley rats. We hypothesized that CIH and OVX would increase ΔFosB in central autonomic regions associated with increases in blood pressure. Intact (INT) and OVX adult female Sprague-Dawley rats were exposed to 7 days of CIH only during the light (sleep) phase or continuous normoxia (CON). Mean arterial pressure (MAP) was continuously monitored by radiotelemetry. Rats were anesthetized with Inactin and euthanized, and brains were collected and processed for immunohistochemistry. CIH increased MAP relative to CON during the light phase, regardless of gonadal status. During the dark (active) phase, an increase in MAP was observed in OVX but not INT rats, irrespective of CIH. CIH significantly increased ΔFosB immunoreactive cells in the caudal nucleus of the solitary tract, A5 region, and rostral ventrolateral medulla regardless of OVX. Independent of CIH, OVX significantly increased ΔFosB immunoreactive cells in the organum vasculosum of the lamina terminalis, median preoptic nucleus, rostral NTS, and the dorsal, medial, and lateral parvocellular subdivisions of the paraventricular nucleus. Our data indicate that CIH and OVX increase blood pressure independently and exert region-specific effects on ΔFosB immunoreactivity in central autonomic regions.
Keywords: Chronic intermittent hypoxia; Delta FosB; central autonomic; estrogen; hypertension; ovariectomy; sex hormone; sympathetic activity.