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Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats.
Am J Physiol Heart Circ Physiol. 2014 May 15; 306(10):H1472-80.AJ

Abstract

We investigated the involvement of nitric oxide (NO) and reactive oxygen species (ROS) on autonomic cardiovascular parameters, vascular reactivity, and endothelial cells isolated from aorta of monosodium glutamate (MSG) obese rats. Obesity was induced by administration of 4 mg/g body wt of MSG or equimolar saline [control (CTR)] to newborn rats. At the 60th day, the treatment was started with N(G)-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg) or 0.9% saline. At the 90th day, after artery catheterization, mean arterial pressure (MAP) and heart rate were recorded. Plasma was collected to assess lipid peroxidation. Endothelial cells isolated from aorta were evaluated by flow cytometry and fluorescence intensity (FI) emitted by NO-sensitive dye [4,5-diaminofluoresceindiacetate (DAF-2DA)] and by ROS-sensitive dye [dihydroethidium (DHE)]. Vascular reactivity was made by concentration-response curves of acetylcholine. MSG showed hypertension compared with CTR. Treatment with L-NAME increased MAP only in CTR. The MSG induced an increase in the low-frequency (LF) band and a decrease in the high-frequency band of pulse interval. L-NAME treatment increased the LF band of systolic arterial pressure only in CTR without changes in MSG. Lipid peroxidation levels were higher in MSG and were attenuated after L-NAME. In endothelial cells, basal FI to DAF was higher in CTR than in MSG. In both groups, acetylcholine increased FI for DAF from basal. The FI baseline to DHE was higher in MSG than in CTR. Acetylcholine increased FI to DHE in the CTR group, but decreased in MSG animals. We suggest that reduced NO production and increased production of ROS may contribute to hypertension in obese MSG animals.

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Authors+Show Affiliations

da Cunha NV
Department of Physiological Sciences State University of Londrina, Londrina, PR;
Pinge-Filho P
Department of Pathological Sciences State University of Londrina, Londrina, PR;
Panis C
Department of Pathological Sciences State University of Londrina, Londrina, PR;
Silva BR
Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil; and.
Pernomian L
Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil; and.
Grando MD
Faculty of Pharmaceutical Sciences of Ribeirão Preto, Department of Physics and Chemistry, University of São Paulo, Ribeirão Preto, SP, Brazil.
Cecchini R
Department of Pathological Sciences State University of Londrina, Londrina, PR;
Bendhack LM
Faculty of Pharmaceutical Sciences of Ribeirão Preto, Department of Physics and Chemistry, University of São Paulo, Ribeirão Preto, SP, Brazil.
Martins-Pinge MC
Department of Physiological Sciences State University of Londrina, Londrina, PR; martinspinge@uel.br.

MeSH

AnimalsBlood PressureDisease Models, AnimalEndothelium, VascularEnzyme InhibitorsHeart RateHypertensionMaleNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide Synthase Type IIIObesityOxidative StressRatsRats, WistarReactive Oxygen SpeciesSodium GlutamateSympathetic Nervous System

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24633548

Citation

da Cunha, Natalia Veronez, et al. "Decreased Endothelial Nitric Oxide, Systemic Oxidative Stress, and Increased Sympathetic Modulation Contribute to Hypertension in Obese Rats." American Journal of Physiology. Heart and Circulatory Physiology, vol. 306, no. 10, 2014, pp. H1472-80.
da Cunha NV, Pinge-Filho P, Panis C, et al. Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats. Am J Physiol Heart Circ Physiol. 2014;306(10):H1472-80.
da Cunha, N. V., Pinge-Filho, P., Panis, C., Silva, B. R., Pernomian, L., Grando, M. D., Cecchini, R., Bendhack, L. M., & Martins-Pinge, M. C. (2014). Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats. American Journal of Physiology. Heart and Circulatory Physiology, 306(10), H1472-80. https://doi.org/10.1152/ajpheart.00520.2013
da Cunha NV, et al. Decreased Endothelial Nitric Oxide, Systemic Oxidative Stress, and Increased Sympathetic Modulation Contribute to Hypertension in Obese Rats. Am J Physiol Heart Circ Physiol. 2014 May 15;306(10):H1472-80. PubMed PMID: 24633548.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats. AU - da Cunha,Natalia Veronez, AU - Pinge-Filho,Phileno, AU - Panis,Carolina, AU - Silva,Bruno Rodrigues, AU - Pernomian,Laena, AU - Grando,Marcella Daruge, AU - Cecchini,Rubens, AU - Bendhack,Lusiane Maria, AU - Martins-Pinge,Marli Cardoso, Y1 - 2014/03/14/ PY - 2014/3/18/entrez PY - 2014/3/19/pubmed PY - 2014/8/15/medline KW - autonomic KW - endothelium KW - monosodium glutamate KW - nitric oxide synthase SP - H1472 EP - 80 JF - American journal of physiology. Heart and circulatory physiology JO - Am J Physiol Heart Circ Physiol VL - 306 IS - 10 N2 - We investigated the involvement of nitric oxide (NO) and reactive oxygen species (ROS) on autonomic cardiovascular parameters, vascular reactivity, and endothelial cells isolated from aorta of monosodium glutamate (MSG) obese rats. Obesity was induced by administration of 4 mg/g body wt of MSG or equimolar saline [control (CTR)] to newborn rats. At the 60th day, the treatment was started with N(G)-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg) or 0.9% saline. At the 90th day, after artery catheterization, mean arterial pressure (MAP) and heart rate were recorded. Plasma was collected to assess lipid peroxidation. Endothelial cells isolated from aorta were evaluated by flow cytometry and fluorescence intensity (FI) emitted by NO-sensitive dye [4,5-diaminofluoresceindiacetate (DAF-2DA)] and by ROS-sensitive dye [dihydroethidium (DHE)]. Vascular reactivity was made by concentration-response curves of acetylcholine. MSG showed hypertension compared with CTR. Treatment with L-NAME increased MAP only in CTR. The MSG induced an increase in the low-frequency (LF) band and a decrease in the high-frequency band of pulse interval. L-NAME treatment increased the LF band of systolic arterial pressure only in CTR without changes in MSG. Lipid peroxidation levels were higher in MSG and were attenuated after L-NAME. In endothelial cells, basal FI to DAF was higher in CTR than in MSG. In both groups, acetylcholine increased FI for DAF from basal. The FI baseline to DHE was higher in MSG than in CTR. Acetylcholine increased FI to DHE in the CTR group, but decreased in MSG animals. We suggest that reduced NO production and increased production of ROS may contribute to hypertension in obese MSG animals. SN - 1522-1539 UR - https://www.unboundmedicine.com/medline/citation/24633548/Decreased_endothelial_nitric_oxide_systemic_oxidative_stress_and_increased_sympathetic_modulation_contribute_to_hypertension_in_obese_rats_ L2 - https://journals.physiology.org/doi/10.1152/ajpheart.00520.2013?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -