Effect of Chronic Inhibition of Nitric Oxide on Hypertension, Insulin Resistance, and Cardiovascular Remodeling in Glucose-fed Rats
| Autor: | Rong Wu, Jacques de Champlain, Réjean Couture, Julie-Émilie Huot-Marchand, Denis deBlois, M. Pilon |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Male
medicine.medical_specialty Epinephrine Aorta Thoracic Blood Pressure Nitric Oxide Muscle Smooth Vascular Nitric oxide Muscle hypertrophy Rats Sprague-Dawley Norepinephrine chemistry.chemical_compound Insulin resistance Superoxides Internal medicine medicine Hyperinsulinemia Animals Ventricular remodeling Pharmacology Ventricular Remodeling biology business.industry Myocardium Hypertrophy Smooth muscle hyperplasia medicine.disease Diet Rats Nitric oxide synthase Oxidative Stress Glucose NG-Nitroarginine Methyl Ester Endocrinology Blood pressure chemistry Hypertension biology.protein Insulin Resistance Nitric Oxide Synthase Cardiology and Cardiovascular Medicine business |
| Zdroj: | Journal of Cardiovascular Pharmacology. 53:405-413 |
| ISSN: | 0160-2446 |
| DOI: | 10.1097/fjc.0b013e3181a1d88a |
| Popis: | To determine the contribution of nitric oxide (NO) in cardiovascular remodeling associated to hypertension and insulin resistance, male Sprague-Dawley rats received tap water supplemented or not (control), with 10% D-glucose (G) and/or 50 mg x kg(-1) x d(-1) L-NAME to inhibit NO synthase (G-LN or LN) for 4 weeks. Systolic blood pressure increased by 12%, 26%, and 39% with G, LN, and G-LN treatments, respectively. Hyperinsulinemia and insulin resistance (homeostasis model assessment index) occurred in G-treated rats (P < 0.05) and were further increased in G-LN (P < 0.01). Plasma adrenaline concentrations were markedly increased in all treated groups, especially in G-LN (P < 0.01), whereas noradrenaline was increased in G-treated rats only. Whereas no cardiac hypertrophy or fibrosis was detected, aortic hypertrophy occurred in LN and G-LN rats (P < 0.001) without smooth muscle hyperplasia. Superoxide anion formation was increased in the aorta of all treated groups (P < 0.01) and in the heart of LN (P < 0.05), but reduced nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase activity was not affected. In conclusion, the loss of the wide-range protective effects of NO, the increased vascular oxidative stress, and the sympathoadrenal hyperactivity are among the contributing factors leading to the exacerbation of hypertension and insulin resistance in G-LN. These factors were sufficient to cause vascular but not cardiac hypertrophy. |
| Databáze: | OpenAIRE |
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