Effects of simulated hyperglycemia, insulin, and glucagon on endothelial nitric oxide synthase expression
| Autor: | Yaoxian Ding, Vaijinath S. Kamanna, Daeyoung D. Roh, Richard Coulson, Nosratola D. Vaziri |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
medicine.medical_specialty
Nitric Oxide Synthase Type III Physiology Endocrinology Diabetes and Metabolism medicine.medical_treatment Glucagon Nitric oxide Insulin Antagonists chemistry.chemical_compound Enos Physiology (medical) Internal medicine Humans Insulin Medicine Endothelial dysfunction Cells Cultured biology business.industry Osmolar Concentration medicine.disease biology.organism_classification Endothelial stem cell Nitric oxide synthase Glucose Endocrinology chemistry Hyperglycemia biology.protein Nitric Oxide Synthase business |
| Zdroj: | American Journal of Physiology-Endocrinology and Metabolism. 279:E11-E17 |
| ISSN: | 1522-1555 0193-1849 |
| DOI: | 10.1152/ajpendo.2000.279.1.e11 |
| Popis: | Diabetes is associated with endothelial dysfunction and increased risk of hypertension, cardiovascular disease, and renal complications. Earlier studies have revealed that hyperglycemia impairs nitric oxide (NO) production and diabetes causes endothelial dysfunction in humans and experimental animals. This study was designed to test the effects of altered concentrations of glucose, insulin, and glucagon, the principal variables in types I and II diabetes, on NO production and endothelial NO synthase (eNOS) expression in cultured human coronary endothelial cells. Cultured endothelial cells were incubated in the presence of glucose at either normal (5.6 mM) or high (25 mM) concentrations for 7 days. The rates of basal and bradykinin-stimulated NO production (nitrate + nitrite) and eNOS protein expression (Western blot) were then determined at the basal condition and in the presence of insulin (10−8and 10−7M), glucagon (10−8and 10−7M), or both. Incubation with a high-glucose concentration for 7 days significantly downregulated, whereas insulin significantly upregulated, basal and bradykinin-stimulated NO production and eNOS expression in cultured endothelial cells. The stimulatory action of insulin was mitigated by high-glucose concentration and abolished by cotreatment of cells with glucagon. Thus hyperglycemia, insulinopenia, and hyperglucagonemia, which frequently coexist in diabetes, can work in concert to suppress NO production by human coronary artery endothelial cells. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|