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Chronic intermittent hypoxia (CIH, 3d) attenuates glutathione peroxidase expression (Gpx1) and function in the caudal nucleus tractus solitarii (cnTS)
Author(s) -
Barr Stacy L.,
Phaup J. Glenn,
Kline David D.,
Hasser Eileen M.,
Heesch Cheryl M.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.697.31
Subject(s) - endocrinology , medicine , splanchnic , gpx1 , hypoxia (environmental) , chemistry , glutathione peroxidase , hemodynamics , superoxide dismutase , oxygen , oxidative stress , organic chemistry
Hypoxia increases reactive oxygen species (ROS) in the nTS which likely contribute to changes in cardiorespiratory control. Previously we reported that 2 h of acute hypoxia increased mRNA for the ROS inactivating enzyme Gpx1 in the nTS. Current experiments evaluated GPX in CIH (3d). Gpx1 mRNA in the cnTS trended to decrease in 6 CIH (0.6 ± 0.1) versus 6 normoxic (N) male rats (1.0 ± 0.3). In inactin anesthetized, neuromuscular blocked, artificially ventilated and vagotomized N (6) and CIH rats (5), baseline cardiorespiratory values were similar. Microinjection of mercaptosuccinic acid (MCS, 30 nl; 0.05, 0.1, 0.5M), a GPX antagonist, in the cnTS produced similar graded responses. At 0.5M, MCS eliminated phrenic nerve discharge, and decreased mean arterial pressure ( N = −50 ± 5; CIH = −45 ± 5 mmHg) and heart rate ( N = −50 ± 5; CIH = −39 ± 9 bpm). However, decreases in splanchnic sympathetic nerve activity due to 0.5M MCS were attenuated in CIH (−68 ± 8%) versus N rats (−87± 4%), consistent with decreased Gpx1 mRNA. Data suggest that an initial compensatory increase in Gpx1 mRNA is reversed following 3 d CIH possibly contributing to attenuated sSNA responses to GPX blockade. NIH HL 98602