Role of Nitric Oxide in Thermoregulation and Hypoxic Ventilatory Response in Obese Zucker Rats

2001 ◽  
Vol 164 (3) ◽  
pp. 437-442 ◽  
Author(s):  
HITOSHI NAKANO ◽  
SHIN-DA LEE ◽  
ANDREW D. RAY ◽  
JOHN A. KRASNEY ◽  
GASPAR A. FARKAS
2014 ◽  
Vol 2 (1) ◽  
Author(s):  
Priyanka Prathipati ◽  
Syed Quadri ◽  
Debra Jackson ◽  
Keith Jackson

PLoS ONE ◽  
2012 ◽  
Vol 7 (4) ◽  
pp. e36027 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
María Pilar Martínez ◽  
Belén Climent ◽  
Sara Benedito ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Martina Cebova ◽  
Radoslava Rehakova ◽  
Michaela Kosutova ◽  
Olga Pechanova

Current treatments for cardiovascular and obesity-associated diseases, such as statin therapy, may be associated with several side effects. Products from food sources with polyphenolic compounds may represent promising agents in the treatment of cardiovascular and metabolic diseases with minimal side effects. Thus, we aimed to study the effect of sesame oil and simvastatin treatment on plasma lipid profile, nitric oxide generation, and oxidative load in obese Zucker rats. 12-week-old male Zucker rats were divided into the control and sesame oil- (1.25 ml/kg/day) treated Zucker lean groups, the control and sesame oil (1.25 ml/kg/day), or simvastatin (15 mg/kg/day) together with sesame oil-treated Zucker fa/fa groups, n=6 in each group. The treatment lasted for 6 weeks. Sesame oil composition and plasma lipid profile were analyzed. Nitric oxide synthase (NOS) activity, endothelial NOS (eNOS), phosphorylated eNOS, and inducible NOS (iNOS) protein expressions were determined in the left ventricle and aorta. Oxidative load, measured as conjugated diene (CD) and thiobarbituric acid reactive substance (TBARS) concentrations, was detected in the liver. Neither sesame oil nor cotreatment with simvastatin affected plasma lipid profile in Zucker fa/fa rats. Sesame oil and similarly cotreatment with simvastatin markedly increased NOS activity and phosphorylated eNOS protein expressions in the left ventricle and aorta of Zucker fa/fa rats. There were no changes in eNOS and iNOS protein expressions within the groups and tissues investigated. Hepatic CD concentration was higher in Zucker fa/fa comparing Zucker lean rats, and sesame oil treatment decreased it significantly. Interestingly, this decrease was not seen after cotreatment with simvastatin. In conclusion, phosphorylation of eNOS and decreased oxidative load may significantly contribute to increase in total NOS activity with potential beneficial properties. Interestingly, simvastatin did not affect NO generation already increased by sesame oil in obese Zucker rats.


2014 ◽  
Vol 11 (6) ◽  
pp. 1463-1474 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
Pilar Martínez ◽  
Mercedes Muñoz ◽  
Ana Cristina Martínez ◽  
...  

2018 ◽  
Vol 152 ◽  
pp. 114-128 ◽  
Author(s):  
Ana Sánchez ◽  
Cristina Contreras ◽  
Belén Climent ◽  
Alejandro Gutiérrez ◽  
Mercedes Muñoz ◽  
...  

Surgery ◽  
2004 ◽  
Vol 136 (3) ◽  
pp. 677-685 ◽  
Author(s):  
George S. Dikdan ◽  
Salim C. Saba ◽  
Andrew N. dela Torre ◽  
Jonathan Roth ◽  
Shulun Wang ◽  
...  

2018 ◽  
Vol 103 (8) ◽  
pp. 1067-1075 ◽  
Author(s):  
Carol T. Bussey ◽  
H. P. Aye Thaung ◽  
Gillian Hughes ◽  
Andrew Bahn ◽  
Regis R. Lamberts

1998 ◽  
Vol 85 (1) ◽  
pp. 129-132 ◽  
Author(s):  
David Gozal

In humans, the hypoxic ventilatory response (HVR) is augmented when preceded by a short hyperoxic exposure (Y. Honda, H. Tani, A. Masuda, T. Kobayashi, T. Nishino, H. Kimura, S. Masuyama, and T. Kuriyama. J. Appl. Physiol. 81: 1627–1632, 1996). To examine whether neuronal nitric oxide synthase (nNOS) is involved in such hyperoxia-induced HVR potentiation, 17 male Sprague-Dawley adult rats underwent hypoxic challenges (10% O2-5% CO2-balance N2) preceded either by 10 min of room air (−O2) or of 100% O2(+O2). At least 48 h later, similar challenges were performed after the animals received the selective nNOS inhibitor 7-nitroindazole (25 mg/kg ip). In −O2 runs, minute ventilation (V˙e) increased from 121.3 ± 20.5 (SD) ml/min in room air to 191.7 ± 23.8 ml/min in hypoxia ( P< 0.01). After +O2,V˙e increased from 114.1 ± 19.8 ml/min in room air to 218.4 ± 47.0 ml/min in hypoxia (+O2 vs. −O2: P < 0.005, ANOVA). After 7-nitroindazole administration, HVR was not affected in the −O2 treatment group withV˙e increasing from 113.7 ± 17.8 ml/min in room air to 185.8 ± 35.0 ml/min in hypoxia ( P < 0.01). However, HVR potentiation in +O2-exposed animals was abolished (111.8 ± 18.0 ml/min in room air to 184.1 ± 35.6 ml/min in hypoxia; +O2 vs. −O2: P not significant). We conclude that in the conscious rat nNOS activation mediates essential components of the HVR potentiation elicited by a previous short hyperoxic exposure.


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