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PARTICIPATION OF NITRIC OXIDE AND PROSTAGLANDINS IN THE CARDIOVASCULAR PARAMETERS OF MSG OBESE RAT
Author(s) -
MartinsPinge Marli Cardoso,
Cunha Natália Veronez,
Abreu Samantha Bagolan,
Grassiolli Sabrina,
PingeFilho Phileno
Publication year - 2009
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.23.1_supplement.1017.8
Subject(s) - medicine , mean arterial pressure , blood pressure , nitric oxide , heart rate , endocrinology , prostacyclin , hemodynamics , prostaglandin , tachycardia , prostaglandin e2 , anesthesia , cardiology
The circulating levels of the cytokines, interleukin and of inflammatory mediators such as prostaglandin, amongst others, are elevated in obese individuals. Also, clinical and experimental data support a link between endothelial dysfunction and inflammation. The aim of this study was to evaluate the effects of 30 days treatment with prostaglandins and nitric oxide inhibitors in the development of obesity induced by neonatal Monosodium Glutamate (MSG) administration upon blood pressure and heart rate in conscious animals. Control or msg obese 90‐day‐old male Wistar rats were anesthetized to femoral artery and vein catheterization for recording mean arterial pressure (MAP) and heart rate (HR) in a conscious state preparation. 24 hours later MAP and HR parameters were analysed by one hour. Obese rats presented hypertension (MAP= 150±1 mmHg) and tachycardia (HR=432±15 bpm) compared with control animals (MAP=116±6 mmHg; HR=334±17 bpm). After treatment with celecoxib, the hypertension was attenuated (MAP=128±2 mmHg; HR=393±21 bpm). The treatment with L‐NAME did not modify MAP parameter (MAP=143±7 mmHg). Our data showed that msg obese rat is also a model of hypertension; which cause may involve at least in part the participation of prostaglandins.