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Chronic hypoxia decreases response to central chemoreceptor stimulation in the nucleus tractus solitarius (NTS)
Author(s) -
Wilkinson Katherine A.,
Nichols Nicole L.,
Putnam Robert W.,
Powell Frank L.
Publication year - 2009
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.23.1_supplement.621.16
Subject(s) - chemoreceptor , acetazolamide , hyperventilation , microinjection , central chemoreceptors , brainstem , stimulation , chemistry , hypoxia (environmental) , anesthesia , hypoxic ventilatory response , peripheral chemoreceptors , dilator , hypercarbia , endocrinology , medicine , respiration , solitary nucleus , acidosis , anatomy , oxygen , receptor , organic chemistry
One hallmark of acclimatization to chronic hypoxia (CH) is hyperventilation and a lower arterial carbon dioxide (CO 2 ) level. These effects persist upon return to normoxia, suggesting a change in the regulation of CO 2 during CH. We tested the hypothesis that plasticity in one central chemoreceptor site, the NTS, contributes to altered CO 2 regulation in CH. In urethane‐anesthetized rats, we stimulated chemoreceptors in the NTS by a unilateral microinjection of acetazolamide (ACZ, 1 nl of 0.3 μM), to produce focal acidosis. The product of rectified, integrated phrenic nerve amplitude and frequency (Phr) was measured 30 min after ACZ in normoxic control (N; n=5) and CH rats (n=5). ACZ increased Phr significantly more in N rats than CH rats (N=263±14%; CH=83±18%; p<0.001). ACZ in adjacent brainstem regions had no effect on Phr. All rats showed the capacity to increase Phr to a 10% inspired CO 2 challenge following ACZ, suggesting that the dose of ACZ did not produce a maximal phrenic response. These results indicate plasticity in chemosensitivity in the NTS but they cannot easily explain the lower CO 2 set point with CH. Supported by NIH HL81823 (FLP) and AHA 0615069Y (KAW).