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EFFECTS OF ENDOTHELIAL NOS ANTAGONISM ON ENDOTHELIAL NOS EXPRESSION WITHIN THE VENTROLATERAL MEDULLA AND CARDIOVASCULAR RESPONSES DURING STATIC SKELETAL MUSCLE CONTRACTION
Author(s) -
Kabadi Shruti,
Phattanarudee Siripan,
Patel Maitreyee,
Maher Timothy John,
Ally Ahmmed
Publication year - 2007
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.21.5.a567-d
Subject(s) - rostral ventrolateral medulla , enos , medicine , endocrinology , endothelial nos , nitric oxide synthase , antagonist , medulla , chemistry , reflex , nitric oxide , medulla oblongata , central nervous system , receptor
We have previously shown that blockade of endothelial nitric oxide synthase (eNOS) 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 ( Neuroscience Research 52 :–30, 2005). In this study, we determined if microdialyzing a specific eNOS antagonist into the RVLM and CVLM would affect cardiovascular responses via molecular changes in eNOS protein expression during the exercise pressor reflex using anesthetized rats. Bilateral microdialysis of a selective eNOS antagonist, 7‐nitroindazole (1μM), for 120 min into the RVLM potentiated cardiovascular responses during a static muscle contraction. At the end of the experiment, western blot analysis of eNOS within both RVLM showed a significant attenuation of the protein expression when compared to control animals microdialyzed with vehicle. In contrast, bilateral application of the drug into the CVLM attenuated cardiovascular responses during muscle contractions. There was an increased eNOS protein expression within the CVLM. These results demonstrated that the molecular mechanism by which eNOS antagonism within the RVLM and CVLM modulated the exercise pressor reflex was via altering eNOS protein expressions.