| InChI=1S/C2H6N2O3/c3-1-2-7-4(5)6/h1-3H2 |
| KZTZJUQNSSLNAG-UHFFFAOYSA-N |
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Bronsted base
A molecular entity capable of accepting a hydron from a donor (Bronsted acid).
(via organic amino compound )
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vasodilator agent
A drug used to cause dilation of the blood vessels.
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View more via ChEBI Ontology
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aminoethyl nitrate
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WHO MedNet
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aminoethylis nitras
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WHO MedNet
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nitrate d'aminoéthyle
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WHO MedNet
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nitrato de aminoetilo
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WHO MedNet
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2-aminoethanol nitrate ester
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ChEBI
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2-nitratoethylamine
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ChEBI
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CLC 1011
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ChEBI
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CLC-1011
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ChEBI
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itramin
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DrugBank
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monoethanolamine nitrate ester
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ChEBI
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nitrolamine
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ChemIDplus
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646-02-6
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CAS Registry Number
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ChemIDplus
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Oelze M, Welschof P, Knorr M, Tran LP, Ullmann E, Stamm P, Kröller-Schön S, Jansen T, Kopp M, Schulz E, Gori T, Burgin K, Scherhag A, Sartor D, Münzel T, Daiber A (2018)
Basic in vitro Characterization of the Vasodilatory Potential of 2-Aminoethyl Nitrate Fixed-Dose Combinations with Cilostazol, Metoprolol and Valsartan.
Pharmacology 101, 54-63 [PubMed:28988245]
[show Abstract]
Background/aims2-aminoethyl nitrate (CLC-1011) is a member of the class of organic nitrates that cause vasodilation by the generation of nitric oxide (•NO). These drugs are mainly used for the treatment of angina pectoris and ischemic heart disease. The aim of this study was to characterize the vasodilatory potency of this organic nitrate alone and in combination with clinically established cardiovascular drugs.MethodsVasodilation by CLC-1011 was tested by isometric tension studies, either alone or combined with cilostazol, valsartan, and metoprolol. Induction of oxidative stress in isolated heart mitochondria was measured by enhanced chemiluminescence. Bioactivation of CLC-1011 in aortic tissue was measured by electron paramagnetic resonance spectroscopy using an iron-based spin trap for •NO.ResultsWe observed potent vasodilation by CLC-1011 and additive effects for all three drug combinations. In contrast to nitroglycerin (GTN), CLC-1011 did not stimulate mitochondrial oxidative stress. CLC-1011 was bioactivated to •NO in aortic tissue.ConclusionIn summary, the experiments described in this report demonstrate that CLC-1011 does not induce oxidative stress, is a more potent vasodilator than isosorbide-5-mononitrate and dinitrate ISDN, and displays synergistic vasodilation with other cardiovascular drugs. CLC-1011 fixed dose combinations could be used in the management of cardiovascular diseases. | McGrath JC (2013)
2-Aminoethylnitrate: Earlier investigation as a drug was missed by recent authors due to changes in nomenclature.
British journal of pharmacology 169, 949-950 [PubMed:23711023] | Uppu S (2013)
2-Aminoethylnitrate: pharmacological uses rediscovered and claimed as original.
British journal of pharmacology 169, 950 [PubMed:23711024] | Bauersachs J (2009)
Aminoethyl nitrate--the novel super nitrate?
British journal of pharmacology 158, 507-509 [PubMed:19732062]
[show Abstract]
Long-term use of most organic nitrates is limited by development of tolerance, induction of oxidative stress and endothelial dysfunction. In this issue of the BJP, Schuhmacher et al. characterized a novel class of organic nitrates with amino moieties (aminoalkyl nitrates). Aminoethyl nitrate was identified as a novel organic mononitrate with high potency but devoid of induction of mitochondrial oxidative stress. Cross-tolerance to nitroglycerin or the endothelium-dependent agonist acetylcholine after in vivo treatment was not observed. Like all nitrates, aminoethyl nitrate induced vasorelaxation by activation of soluble guanylate cyclase. Thus, in contrast to the prevailing view, high potency in an organic nitrate is not necessarily accompanied by induction of oxidative stress or endothelial dysfunction. This work from Daiber's group is an important step forward in the understanding of nitrate bioactivation, tolerance phenomena and towards the development of better organic nitrates for clinical use. | Plets C (1989)
Arterial hypertension in neurosurgical emergencies.
The American journal of cardiology 63, 40C-42C [PubMed:2913756]
[show Abstract]
The Cushing, or ischemic response, is a useful mechanism in intracranial hypertension because it restores normal cerebral perfusion pressure and cerebral circulation. In patients with acute intracranial hypertension due to mass-expanding lesions such as brain edema, hydrocephalus or brain tumor, cerebral perfusion pressure decreases and plateau waves occur. In experimental animals, spontaneous or induced arterial hypertension can compensate for the reduction of cerebral perfusion pressure. The interrelation between arterial pressure, intracranial pressure and cerebral perfusion pressure in an experimental model of hydrocephalus in dogs was investigated. Plateau waves were preceded by a decrease in cerebral perfusion pressure and a Cushing response was seen 5 to 15 seconds before abolition of the wave. Arterial hypertension, induced by intravenous infusion of Aramin, restored cerebral perfusion pressure and intracranial pressure became normal. Arterial hypertension appears to be an efficient stimulus to abort plateau waves. Hypertensive patients in whom subarachnoid bleeding develops from ruptured aneurysm are at high risk of bleeding again and need antihypertensive treatment together with drainage of cerebrospinal fluid. Induced arterial hypertension is the most effective treatment of vasospasm but increases the danger of aneurysmal rebleeding and can only be safe after clipping of the aneurysm. This is one of the strongest arguments for early operation on cerebral aneurysms. |
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