PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16101430-1 2005 Organic nitrates, such as nitroglycerin, have been used in clinical practice for more than one century for the treatment of angina, even before the identification of Nitric Oxide (NO) as the so-called Endothelium Derived Relaxing Factor (EDRF). Nitrates 8-16 alpha hemoglobin stabilizing protein Homo sapiens 238-242 9211013-2 1997 Additional efficacy stems from the ability of the nitrates to replenish the deficient endothelium-derived relaxing factor (EDRF), nitric oxide (NO), in patients with coronary heart disease and also to inhibit platelet aggregation. Nitrates 50-58 alpha hemoglobin stabilizing protein Homo sapiens 86-121 10684481-2 1998 When nitrates are metabolized to release NO, there is a considerable coproduction of reactive oxygen species (superoxide radical and peroxynitrite) in vessels leading to inactivation of NO, to diminished cyclic quanosine monophosphate production in smooth muscle cells (SMC), to impaired vasomotor responses to the endothelium-derived relaxation factor (EDRF), and to formation of nitrotyrosine as a marker of glyceryltrinitrate (GTN)-induced formation of peroxynitrite. Nitrates 5-13 alpha hemoglobin stabilizing protein Homo sapiens 315-352 10684481-2 1998 When nitrates are metabolized to release NO, there is a considerable coproduction of reactive oxygen species (superoxide radical and peroxynitrite) in vessels leading to inactivation of NO, to diminished cyclic quanosine monophosphate production in smooth muscle cells (SMC), to impaired vasomotor responses to the endothelium-derived relaxation factor (EDRF), and to formation of nitrotyrosine as a marker of glyceryltrinitrate (GTN)-induced formation of peroxynitrite. Nitrates 5-13 alpha hemoglobin stabilizing protein Homo sapiens 354-358 16793713-1 1998 Limited information seems to be available about the role of reduced endothelial production of endotheliumderived relaxing factor (EDRF)-nitrate/nitrite (NO) in the pathogenesis of diabetic angiopathy in insulindependent diabetes. Nitrates 136-143 alpha hemoglobin stabilizing protein Homo sapiens 94-128 16793713-1 1998 Limited information seems to be available about the role of reduced endothelial production of endotheliumderived relaxing factor (EDRF)-nitrate/nitrite (NO) in the pathogenesis of diabetic angiopathy in insulindependent diabetes. Nitrates 136-143 alpha hemoglobin stabilizing protein Homo sapiens 130-134 9211013-2 1997 Additional efficacy stems from the ability of the nitrates to replenish the deficient endothelium-derived relaxing factor (EDRF), nitric oxide (NO), in patients with coronary heart disease and also to inhibit platelet aggregation. Nitrates 50-58 alpha hemoglobin stabilizing protein Homo sapiens 123-127 3154691-12 1988 Therefore nitrates may particularly be effective in vessels with deficient EDRF release. Nitrates 10-18 alpha hemoglobin stabilizing protein Homo sapiens 75-79 9175238-10 1997 In IDDM the decreased nitrate/nitrite excretion may also lead to increased in vivo platelet activation, which suggests that the reduced amount of EDRF-NO might play a role in the pathogenesis of angiopathy in IDDM. Nitrates 22-29 alpha hemoglobin stabilizing protein Homo sapiens 146-150 8248688-4 1993 In parallel with the discovery of the endothelium-derived relaxing factor (EDRF) and its biochemical identification as nitric oxide (NO), it became clear that organic nitrates act via the release of NO in the vascular wall and thus by using metabolic pathways identical to those of endogenous EDRF. Nitrates 167-175 alpha hemoglobin stabilizing protein Homo sapiens 75-79 8248688-4 1993 In parallel with the discovery of the endothelium-derived relaxing factor (EDRF) and its biochemical identification as nitric oxide (NO), it became clear that organic nitrates act via the release of NO in the vascular wall and thus by using metabolic pathways identical to those of endogenous EDRF. Nitrates 167-175 alpha hemoglobin stabilizing protein Homo sapiens 293-297 2577296-2 1989 The recently elucidated mechanism of action of nitrates, acting on a common pathway with the endothelium-derived relaxation factor (EDRF), suggests an important role for guanylate cyclase and cyclic GMP in maintaining coronary artery patency in patients with coronary atheroma. Nitrates 47-55 alpha hemoglobin stabilizing protein Homo sapiens 93-130 2577296-2 1989 The recently elucidated mechanism of action of nitrates, acting on a common pathway with the endothelium-derived relaxation factor (EDRF), suggests an important role for guanylate cyclase and cyclic GMP in maintaining coronary artery patency in patients with coronary atheroma. Nitrates 47-55 alpha hemoglobin stabilizing protein Homo sapiens 132-136 2511690-7 1989 The real clinical importance of nitrates became, however, evident only in the last decade with the discovery of EDRF, the so-called endothelial-derived relaxing factor, an endogenous compound of endothelial origin at least partly consisting of nitrous oxide and therefore, like nitrates, it exerts its effect through the stimulation of cGMP. Nitrates 32-40 alpha hemoglobin stabilizing protein Homo sapiens 112-116 7914830-1 1994 As a result of recent advances in our understanding of the role of nitric oxide and endothelial-derived relaxing factor (EDRF) in vascular control, physicians now have the potential to overcome the loss of EDRF effect by administering nitrates. Nitrates 235-243 alpha hemoglobin stabilizing protein Homo sapiens 84-119 7914830-1 1994 As a result of recent advances in our understanding of the role of nitric oxide and endothelial-derived relaxing factor (EDRF) in vascular control, physicians now have the potential to overcome the loss of EDRF effect by administering nitrates. Nitrates 235-243 alpha hemoglobin stabilizing protein Homo sapiens 121-125 7914830-1 1994 As a result of recent advances in our understanding of the role of nitric oxide and endothelial-derived relaxing factor (EDRF) in vascular control, physicians now have the potential to overcome the loss of EDRF effect by administering nitrates. Nitrates 235-243 alpha hemoglobin stabilizing protein Homo sapiens 206-210 1874272-3 1991 EDRF-NO and NO generated from vasodilator nitrates work by activation of soluble guanylate cyclase, elevating cyclic guanosine monophosphate (GMP) levels to cause vasodilatation and inhibition of platelet aggregation. Nitrates 42-50 alpha hemoglobin stabilizing protein Homo sapiens 0-4 2113002-10 1990 Thus, the administration of low doses of nitrates that act by means of the NO radical can increase the diameter in the stenosis, since the physiological dilator (EDRF) is no longer present. Nitrates 41-49 alpha hemoglobin stabilizing protein Homo sapiens 162-166 2511690-7 1989 The real clinical importance of nitrates became, however, evident only in the last decade with the discovery of EDRF, the so-called endothelial-derived relaxing factor, an endogenous compound of endothelial origin at least partly consisting of nitrous oxide and therefore, like nitrates, it exerts its effect through the stimulation of cGMP. Nitrates 278-286 alpha hemoglobin stabilizing protein Homo sapiens 112-116