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|Title:||Reduction of infarct size by orally administered des-aspartate-angiotensin I in the ischemic reperfused rat heart||Authors:||Wen, Q.
|Issue Date:||2004||Citation:||Wen, Q., Sim, M.-K., Tang, F.-R. (2004). Reduction of infarct size by orally administered des-aspartate-angiotensin I in the ischemic reperfused rat heart. Regulatory Peptides 120 (1-3) : 149-153. ScholarBank@NUS Repository.||Abstract:||Occlusion of the left main coronary artery for 45 min caused sizable infarct scaring of the left ventricular wall in the rat heart at 14 days post-reperfusion. Daily oral administration of des-aspartate-angiotensin I (DAA-I) for 14 days attenuated the area of the infarct scar and transmurality. The attenuation was dose-dependent and biphasic; maximum effective dose was 1524 nmol/kg, and doses higher than this were progressively inactive. The exact mechanism of the biphasic attenuation is not known, and receptor down-regulation by internalization, which has been implicated in a similar biphasic nature for the anticardiac hypertrophic action of DAA-I, could be a likely cause. Indomethacin (101 μmol/kg, i.p.), administered sequentially after the daily oral dose of DAA-I (1524 nmol/kg), completely inhibited the attenuation at 14 days post-reperfusion, indicating that prostaglandins may be involved in transducing the attenuation. The present findings support earlier indications that DAA-I exerts protective actions in cardiovascular pathologies in which angiotensin II is implicated. It is suggested that DAA-I exerts the cardioprotective action by acting on the same indomethacin-sensitive angiotensin AT1 receptor. Although similar array of protective actions are also seen with another endogenous angiotensin, angiotensin-(1-7), the present findings demonstrate for the first time the ability of an endogenous angiotensin to reduce the infarct size of an ischemic-reperfusion injured rat heart. © 2004 Elsevier B.V. All rights reserved.||Source Title:||Regulatory Peptides||URI:||http://scholarbank.nus.edu.sg/handle/10635/33859||ISSN:||01670115|
|Appears in Collections:||Staff Publications|
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