Document Detail


Neuronal nitric oxide synthase (nNOS) blockade within the ventrolateral medulla differentially modulates cardiovascular responses and nNOS expression during static skeletal muscle contraction.
MedLine Citation:
PMID:  17382301     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Nitric oxide (NO) is synthesized from L-arginine through the activity of the enzyme, NO synthase (NOS). Previous studies have demonstrated the role of the 3 isoforms of NOS, namely endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) in cardiovascular regulation. Local blockade of nNOS in RVLM vs. CVLM differentially alters local glutamate and GABA release, and thereby results in opposite cardiovascular responses to static muscle contraction (Brain Res. 2003, 977, 80-89). In this study, we examined whether nNOS antagonism within the RVLM and CVLM affected cardiovascular responses during the exercise pressor reflex and simultaneously modulated medullary nNOS protein expression using anesthetized rats. Bilateral microdialysis of a selective nNOS antagonist, 1-(2-trifluoromethylphenyl)-imidazole (TRIM, 1.0 microM) for 120 min into the RVLM, potentiated cardiovascular responses during a static muscle contraction. Western blot analysis of nNOS expression within the RVLM showed significant attenuation of the protein when compared to the data obtained from control animals microdialyzed with vehicle. In contrast, bilateral application of TRIM into the CVLM attenuated cardiovascular responses during muscle contractions and increased nNOS protein expression within the CVLM. These results demonstrated that nNOS protein expression within the brainstem was pharmacologically altered by nNOS blockade within the RVLM or CVLM, which in turn might have contributed to the augmentation or attenuation of cardiovascular responses, respectively, during static exercise.
Authors:
Ahmmed Ally; Shruti Kabadi; Siripan Phattanarudee; Maitreyee Patel; Timothy J Maher
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2007-03-02
Journal Detail:
Title:  Brain research     Volume:  1150     ISSN:  0006-8993     ISO Abbreviation:  Brain Res.     Publication Date:  2007 May 
Date Detail:
Created Date:  2007-05-14     Completed Date:  2007-07-24     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  21-31     Citation Subset:  IM    
Affiliation:
Department of Pharmaceutical Sciences, Massachusetts College of Pharmacy and Health Sciences, 179 Longwood Avenue, Boston, MA 02115, USA. Ahmmed.Ally@mcphs.edu
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Blood Pressure / drug effects,  physiology
Cardiovascular System* / drug effects
Enzyme Inhibitors / pharmacology
Female
Functional Laterality
Gene Expression Regulation / drug effects,  physiology*
Heart Rate / drug effects,  physiology
Imidazoles / pharmacology
Medulla Oblongata / anatomy & histology,  drug effects,  enzymology*
Muscle Contraction / drug effects,  physiology*
Muscle, Skeletal / drug effects,  physiology*
Nitric Oxide Synthase Type I / genetics,  metabolism*
Physical Conditioning, Animal
Rats
Rats, Sprague-Dawley
Time Factors
Grant Support
ID/Acronym/Agency:
RR-16741/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Imidazoles; 25371-96-4/1-(2-trifluoromethylphenyl)imidazole; EC 1.14.13.39/Nitric Oxide Synthase Type I

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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