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Am J Physiol Heart Circ Physiol 282: H734-H738, 2002; doi:10.1152/ajpheart.00583.2001
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Vol. 282, Issue 2, H734-H738, February 2002

Effect of NO on EDHF response in rat middle cerebral arteries

Lisa A. Schildmeyer1 and Robert M. Bryan Jr.1,2,3

Departments of 1 Anesthesiology, Molecular Physiology, and 2 Biophysics, and 3 Section of Cardiovascular Sciences, Department of Medicine Baylor College of Medicine, Houston, Texas 77030

Whereas the actual identity of endothelium-derived hyperpolarizing factor (EDHF) is still not certain, it involves a process requiring the endothelium and eliciting hyperpolarization and relaxation of smooth muscle. It is neither nitric oxide (NO) nor prostacyclin, and its presence has been demonstrated in a variety of vessels. Recent studies in peripheral vessels report that EDHF-mediated dilations were either attenuated or blocked by NO. Studies presented here demonstrate that NO does not block EDHF-mediated dilations in cerebral vessels. Rat middle cerebral arteries were cannulated, pressurized, and luminally perfused. EDHF-mediated dilations were elicited by the luminal application of ATP in the presence of NG-nitro-L-arginine methyl ester (L-NAME) and indomethacin (inhibitors of NO synthase and cyclooxygenase, respectively). These dilations persisted when S-nitroso-N-acetylpenicillamine, an NO donor, was added exogenously in the presence of L-NAME, or when endogenous NO was present but its cGMP actions were blocked by 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, an inhibitor of guanylate cyclase. These findings demonstrate that the EDHF response is not suppressed by NO in cerebral vessels and suggests a role for EDHF during normal physiological conditions.

nitric oxide; endothelium-derived hyperpolarizing factor; guanosine 3',5'-cyclic monophosphate


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