Abstract
Email: akos.koller@aok.pte.hu In cardio-metabolic diseases both the coronary circulation and cardiac metabolism are altered. We have studied a condition called hyperhomocysteinemia (HHcy), which can develop as a result of genetic or environmental causes. This metabolic disease is underappreciated, yet even mild or moderate elevation of plasma concentrations of homocystein (Hcy, a sulfur-containing amino acid produced via methionine metabolism) leads to coronary and peripheral arterial and vascular diseases, increased thrombosis and consequently increased mortality. The underlying mechanisms have not been revealed yet. Our recent studies indicate that there are common pathomechanisms, which may affect all of the cellular functions involved. We have shown that a dysfunction of nitric oxide (NO) mediation of dilator responses in isolated rat arterioles with methionine diet-induced hyperhomocysteinemia develops (Arterioscler Thromb Vasc Biol. 1999;19(8):1899-904) with simultaneously increased TXA2 the activity in arterioles and platelets (Arterioscler Thromb Vasc Biol. 2000;20(5): 1203-8). This was due to an oxidative stress-induced dysProπireni saaeetak / Extended abstract
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