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DAA-I (des-aspartate-angiotensin-I) is an agonist on the angiotensin AT1 receptor and releases prostaglandins which mediate its actions. DAA-I administer at doses lesser than Km of metabolizing enzymes antagonize the deleterious actions of angiotensin II. DAA-I appear function in vivo as a physiological antagonist to angiotensin II.
Des-aspartate-angiotensin I (DAA-I) is a nine-amino acid angiotensin peptide and a metabolite of angiotensin DAA-I mediates attenuation of early inflammatory processes and intercellular adhesion molecule-1 (ICAM-1) formation in animal models.
保管分類コード
11 - Combustible Solids
WGK
WGK 3
引火点(°F)
Not applicable
引火点(℃)
Not applicable
試験成績書(COA)
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Regulatory peptides, 129(1-3), 213-219 (2005-06-02)
The present study investigated the action of des-aspartate-angiotensin I (DAA-I) on the pressor action of angiotensin II in the renal and mesenteric vasculature of WKY, SHR and streptozotocin (STZ)-induced diabetic rats. Angiotensin II-induced a dose-dependent pressor response in the renal
Drugs in R&D, 16(4), 317-326 (2016-09-30)
Des-aspartate-angiotensin I (DAA-I) is an endogenous angiotensin peptide and a prototype angiotensin receptor agonist (ARA). It acts on the angiotensin AT
PloS one, 10(9), e0138009-e0138009 (2015-09-18)
ACE inhibitors and ARBs (angiotensin receptor blockers) have been shown to attenuate radiation injuries in animal models of lethal gamma irradiation. These two classes of drug act by curtailing the actions of angiotensin II-linked inflammatory pathways that are up-regulated during
Regulatory peptides, 120(1-3), 15-22 (2004-06-05)
An earlier study showed that des-aspartate-angiotensin I (DAA-I) attenuated the pressor action of angiotensin III in aortic rings of the spontaneously hypertensive rat (SHR) but not the normotensive Wistar Kyoto (WKY) rat. The present study investigated similar properties of DAA-I
Regulatory peptides, 188, 40-45 (2013-12-18)
L6 skeletal muscle cells overexpressed ICAM-1 when treated with H2O2. Maximum effect was observed at 200 μM H2O2. Des-aspartate-angiotensin I (DAA-I) concentration-dependently attenuated the overexpression. Maximum attenuation occurred at 10(-10) M DAA-I. H2O2 activated NFκB and its translocation into the
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