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Quantification of the in vivo production of nitric oxide within the nucleus tractus solitarius during activation of the skeletal muscle mechanoreflex
Author(s) -
Leal Anna K,
Cherry Brandon H,
Murphy Megan N,
Squiers John J,
Smith Scott A
Publication year - 2010
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.24.1_supplement.807.2
Subject(s) - nitric oxide , microdialysis , skeletal muscle , stimulation , in vivo , chemistry , anatomy , medicine , endocrinology , biology , microbiology and biotechnology
During exercise, the skeletal muscle mechanoreflex (MMR) evokes increases in blood pressure. Sensory information from the MMR is processed in the nucleus tractus solitarius (NTS). Pharmacological data suggest that MMR function is modulated by the production of nitric oxide (NO) in the NTS. Due to the instability and short half‐life of NO, direct quantification of NO production in the NTS during activation of the MMR has yet to be reported. We recently quantified the in vivo production of NO within the NTS (at rest) using the molecular probe 1,2‐diaminoanthraquinone (DAA). DAA reacts with NO to form a water‐insoluble red‐fluorescent precipitate that can be quantified by microscopic analysis of fixed tissue. The purpose of this study was to determine the changes in NO production in the NTS during MMR activation using the DAA method. Using microdialysis, DAA (100 μg/mL) was delivered bilaterally to the NTS of Sprague‐Dawley rats (n=6) for 15 min at rest or during stimulation of the MMR via passive stretch of hindlimb skeletal muscle. Animals were then fixed and brainstem tissue harvested. As compared to rest, MMR activation significantly enhanced fluorescence by 156±8% and 114±11% within the NTS ipsilateral and contralateral to the stretched muscle, respectively. The data provide direct evidence that NO production is augmented within the NTS in response to stimulation of the MMR. Supported by HL‐094075 and HL‐088422.