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Altered regulation of sympathetic nerve activity by the caudal ventrolateral medulla in rats after exposure to chronic intermittent hypoxia
Author(s) -
Huber Domitila Augusta,
Schreihofer Ann 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.699.5
Subject(s) - rostral ventrolateral medulla , medulla , tonic (physiology) , medulla oblongata , endocrinology , medicine , microinjection , glutamate receptor , chemistry , inhibitory postsynaptic potential , gabaergic , bicuculline , chloralose , stimulation , anesthesia , central nervous system , receptor , gabaa receptor
After exposure to CIH, rats have elevated sympathetic nerve activity (SNA) and arterial pressure (AP). In addition, we have observed that rats exposed to CIH have reduced GABAergic inhibition of rostral ventrolateral medulla (RVLM), the source of drive for SNA. The caudal ventrolateral medulla (CVLM) is the major source of tonic inhibitory input to the RVLM. Here, we determined whether exposure to CIH reduces tonic CVLM‐mediated inhibition of SNA. Rats (8 wks old) were exposed to CIH (6% O2 for 40s, every 9 min, 8h/day, 2 wks). Then rats were ventilated, paralyzed, and prepared to record AP and splanchnic SNA. Under chloralose anesthesia rats subjected to CIH (n=9) vs. controls (n=7) had higher SNA (1.9 ± 0.2 vs. 0.9 ± 0.2 μV, P<0.05). Stimulation of CVLM by microinjection of glutamate (1 nmol/50 nl) virtually eliminated SNA (93 ± 3 vs. 94 ± 3 %) and produced bigger decreases in mean AP in CIH‐exposed rats (−39 ± 4 vs. −21 ± 3 mmHg, P<0.05). In contrast, inhibition of glutamatergic inputs to CVLM (kynurenate; 5.4 nmol/50 nl) evoked smaller rises in SNA in CIH rats (n=9) vs. control rats (n=7; 361 ± 63 vs. 605 ± 84 %, P < 0.05). These results suggest that the higher SNA in rats subjected to CIH can be eliminated by activation of the CVLM, likely via inhibition of an elevated drive from the RVLM. Furthermore, a reduced tonic inhibitory influence from the CVLM may contribute to the elevated SNA observed in rats after CIH. Support: NIHHL075174.