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Wascher, TC; Bachernegg, M; Kickenweiz, A; Stark, G; Stark, U; Toplak, H; Graier, WF.
Involvement of the L-arginine-nitric oxide pathway in hyperglycaemia-induced coronary artery dysfunction of isolated guinea pig hearts.
Eur J Clin Invest. 1996; 26(8):707-712 Doi: 10.1111/j.1365-2362.1996.tb02157.x
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Leading authors Med Uni Graz
Wascher Thomas
Co-authors Med Uni Graz
Graier Wolfgang
Toplak Hermann
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Abstract:
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.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Arginine - metabolism
Blood Circulation - drug effects
Coronary Vessels - metabolism
Diabetes Mellitus, Type 1 - complications
Female - complications
Glucose - pharmacology
Guinea Pigs - pharmacology
Heart Rate - drug effects
Hyperglycemia - metabolism
Indomethacin - pharmacology
Male - pharmacology
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide - metabolism
Perfusion - metabolism
Vascular Resistance - drug effects
Vasodilation - drug effects

Find related publications in this database (Keywords)
Coronary Arteries
Diabetes
Hyperglycemia
L-Arginine
Nitric Oxide
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