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Inducible nitric oxide synthase blockade within the ventrolateral medulla differentially modulates the exercise pressor reflex in stroke rats (681.5)
Author(s) -
Hoppenrath Andrew,
Phillips Michael,
Maher Timothy,
Ally Ahmmed
Publication year - 2014
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.28.1_supplement.681.5
Subject(s) - rostral ventrolateral medulla , reflex , medicine , nitric oxide synthase , endocrinology , microdialysis , medulla , contraction (grammar) , nitric oxide , antagonist , medulla oblongata , chemistry , anesthesia , central nervous system , receptor
We have previously shown that blockade of neuronal nitric oxide synthase (nNOS) within the rostral (RVLM) and caudal ventrolateral medulla (CVLM) differentially modulates cardiovascular responses via changes in glutamate and GABA concentrations during static skeletal muscle contraction. Using left‐sided stroked rats in this study, we determined if microdialyzing a specific iNOS antagonist into the left RVLM and/or the left CVLM would alter cardiovascular responses during static muscle contraction commonly known as the Exercise Pressor Reflex. Rats were stroked by employing a 90 minute left‐sided middle cerebral artery occlusion (MCAO) followed by 24 hours of reperfusion. In protocol 1, microdialysis of a selective iNOS antagonist, aminoguanidine (AGN; 10 µM) for 120 min into the left RVLM significantly attenuated cardiovascular responses during a static muscle contraction compared to those induced in intact rats. In Protocol 2, application of AGN into the left CVLM significantly potentiated the cardiovascular responses during muscle contractions. Finally, in Protocol 3, administration of AGN simultaneously into both the left RVLM and left CVLM produced results similar to those observed with Protocol 1. These results demonstrate that blockade of iNOS within the two regions of the ventrolateral medulla differentially modulates cardiovascular responses during static exercise in stroked rats.