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Involvement of the L‐arginine‐nitric oxide pathway in hyperglycaemia‐induced coronary artery dysfunction of isolated guinea pig hearts
Author(s) -
WASCHER T. C.,
BACHERNEGG M.,
KICKENWEIZ A.,
STARK G.,
STARK U.,
TOPLAK H.,
GRAIER W. F.
Publication year - 1996
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.1996.tb02157.x
Subject(s) - nitric oxide , guinea pig , medicine , arginine , cardiology , artery , endocrinology , pharmacology , chemistry , biochemistry , amino acid
. 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 N G ‐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.