Involvement of the L-arginine-nitric oxide pathway in hyperglycaemia-induced coronary artery dysfunction of isolated guinea pig hearts
| Autor: | T. C. Wascher, A. Kickenweiz, U. Stark, Wolfgang F. Graier, Hermann Toplak, Gerhard Stark, Maria Bachernegg |
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| Rok vydání: | 1996 |
| Předmět: |
Male
medicine.medical_specialty Arginine Guinea Pigs Indomethacin Clinical Biochemistry Vasodilation Nitric Oxide Biochemistry Nitric oxide Guinea pig chemistry.chemical_compound Heart Rate Internal medicine medicine Animals business.industry General Medicine Coronary Vessels Perfusion Coronary arteries Diabetes Mellitus Type 1 Glucose NG-Nitroarginine Methyl Ester medicine.anatomical_structure Endocrinology chemistry Hyperglycemia Blood Circulation Circulatory system Nitric Oxide Pathway Female Vascular Resistance business Blood vessel |
| Zdroj: | Scopus-Elsevier |
| ISSN: | 1365-2362 0014-2972 |
| DOI: | 10.1111/j.1365-2362.1996.tb02157.x |
| Popis: | The effects of hyperglycaemia and L-arginine on flow-induced reduction of coronary artery resistance were investigated in isolated guinea pig hearts. In the presence of indomethacin, hyperglycaemia caused an increase in flow-induced vasodilatation (P < 0.05). Hyperosmotic controls failed to mimic this effect. Addition of L-arginine strongly enhanced this effect. Addition of D-arginine failed to mimic the effects of L-arginine. The effect of L-arginine was abolished by co-administration of NG-nitro-L-arginine. In the absence of indomethacin and L-arginine, the effect of hyperglycaemia was blunted, suggesting the formation of vasoconstrictive prostanoids. Addition of L-arginine again resulted in a significant increase in flow-induced vasodilatation. In conclusion our results suggest that increased flow-induced vasodilatation under hyperglycaemic conditions depends on an adequate supply of L-arginine to maintain sufficient formation of nitric oxide. |
| Databáze: | OpenAIRE |
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