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Exercise pressor reflex dysfunction in hypertension: a role for nitric oxide synthase (NOS) within the nucleus tractus solitarius (NTS)
Author(s) -
Leal Anna K,
Newcomb Richard,
Squiers Jack,
Smith Scott A
Publication year - 2008
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.22.1_supplement.957.20
Subject(s) - endocrinology , medicine , enos , nitric oxide synthase , endothelial nos , nitric oxide , medulla oblongata , reflex , rostral ventrolateral medulla , brainstem , chemistry , central nervous system
An overactive exercise pressor reflex (EPR; a circulatory reflex originating in skeletal muscle) mediates, in part, the exaggerated cardiovascular response to exercise in hypertension. Evidence suggests that decreases in the production of nitric oxide (NO) within the NTS of the medulla oblongata contribute to this EPR dysfunction. The mechanism by which NO production is reduced in the NTS remains unclear. NO is produced by the oxidation of l‐arginine by NOS. Thus, we hypothesized that reductions in NO production are due to the decreased expression of the neuronal (nNOS), endothelial (eNOS) and inducible (iNOS) isoforms of NOS within the NTS. Male, 20 week old, normotensive Wistar Kyoto (WKY; n=3) and spontaneously hypertensive (SHR; n=3) rats were anesthetized and transcardially perfused with 4% paraformaldehyde. Medullary brainstem tissue was harvested and interrogated for NOS protein expression using standard immunohistochemical techniques. Analyses determined that nNOS, eNOS and iNOS expression was markedly reduced in the NTS of SHR as compared to WKY. Although not direct evidence, these findings support the contention that decreases in NO production in hypertension may be due to reductions in NOS expression within the NTS. As such, decreases in NOS protein expression within the NTS may contribute significantly to the development of EPR dysfunction in hypertension. Supported by AHA SDG‐0735355N.