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  • Title: Role of oxidative metabolism on endothelium-dependent vascular relaxation of isolated vessels.
    Author: Cappelli-Bigazzi M, Battaglia C, Pannain S, Chiariello M, Ambrosio G.
    Journal: J Mol Cell Cardiol; 1997 Mar; 29(3):871-9. PubMed ID: 9152848.
    Abstract:
    The obligatory role of endothelium in mediating vasodilator response to numerous humoral agents has been definitely accepted. However, the chemical identity of endothelium-derived relaxing factor(s) (EDRF) and the mechanisms underlying its synthesis and release remain unclear. Much evidence suggests a compartmentalization of ATP into cells, such that ATP derived from glycolysis or from oxidative metabolism is used for different cellular functions. To investigate which energy source (i.e. oxidative v glycolytic metabolism) is preferentially used for the biosynthesis and/or release of EDRF, rings of rabbit thoracic aorta were studied in organ chambers. After preconstriction with PGF2 alpha, inhibition of glycolysis with either iodoacetate (300 microM) (n = 6) or 2-deoxyglucose (20 mM) (n = 6) did not affect concentration-response curve to the endothelium-dependent agent acetylcholine. In contrast, inhibition of oxidative metabolism with either 1 mM amytal or 5 microM rotenone markedly impaired relaxation to acetylcholine. In fact, maximal relaxation was 75 +/- 5% in control rings (n = 6), and 42 +/- 7% (P < 0.01) in amytal-treated rings (n = 6), whereas rotenone converted acetylcholine relaxation into constriction (n = 6; P < 0.001). The effect of amytal on endothelium-dependent relaxation was reversible, suggesting that endothelial cells were not damaged by the inhibitor. Amytal also markedly reduced endothelium-mediated relaxation to ADP (37 +/- 6%; P < 0.05; n = 5), as well as to the calcium ionophore A23187. Neither mitochondrial inhibitor affected relaxation to nitroglycerin, an endothelium-independent agent. Finally, amytal did not affect relaxation to S-nitrosocysteine (a recently proposed EDRF) (n = 5), suggesting that the effects on acetylcholine and ADP responses were not due to non-specific interferences with EDRF once released from endothelial cells. In conclusion, our data demonstrate that the active process of biosynthesis and/or release of EDRF requires energy derived mainly from mitochondrial oxidative metabolism.
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