Astrocytes in NTS after exposure to chronic intermittent hypoxia

Abstract

Chronic intermittent hypoxia (CIH) is a model of the arterial hypoxemia that accompanies sleep apnea and increases resting arterial pressure. Exposures to hypoxia activate astrocytes in the brain. Astrocytes are a primary source of brain angiotensinogen, the precursor to angiotensin II. We tested the hypothesis that chronic intermittent hypoxia increases astrocytes in the nucleus tractus solitarii (NTS). Sprague‐Dawley rats (13 ± 0.3 weeks old) were exposed to CIH (9% oxygen for 3min every 10 min, 8 h per day) for 7 days (n = 5) while control rats (n = 4) were maintained in normoxia. After the CIH protocol, brain stem tissue containing NTS was obtained. Protein levels of the astrocyte marker glial fibrillary acidic protein (GFAP) in the NTS were assessed by Western blot analysis. Relative protein levels of GFAP to actin in the caudal NTS did not differ between CIH and control groups (3.3 ± 1.7 vs. 4.0 ± 1.7, CIH vs. control, P=0.59). The GFAP levels tended to be lower in CIH than in the control group in intermediate and rostral NTS (intermediate: 2.3 ± 1.1 vs. 3.7 ± 0.6, P=0.11; rostral: 1.5 ± 0.9 vs. 2.7 ± 1.0, P=0.052). These results did not support the idea that hypertension induced by CIH is associated with an activation of astrocytes in the NTS. CIH might decrease astrocytes in the NTS as opposed to our hypothesis. Supported by HL‐088052