Please use this identifier to cite or link to this item:
https://doi.org/10.1016/j.regpep.2004.03.003
DC Field | Value | |
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dc.title | Reduction of infarct size by orally administered des-aspartate-angiotensin I in the ischemic reperfused rat heart | |
dc.contributor.author | Wen, Q. | |
dc.contributor.author | Sim, M.-K. | |
dc.contributor.author | Tang, F.-R. | |
dc.date.accessioned | 2012-04-02T07:42:24Z | |
dc.date.available | 2012-04-02T07:42:24Z | |
dc.date.issued | 2004 | |
dc.identifier.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. https://doi.org/10.1016/j.regpep.2004.03.003 | |
dc.identifier.issn | 01670115 | |
dc.identifier.uri | http://scholarbank.nus.edu.sg/handle/10635/32124 | |
dc.description.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. | |
dc.source | Scopus | |
dc.subject | Des-aspartate-angiotensin I | |
dc.subject | Infarct size | |
dc.subject | Ischemia-reperfusion injury | |
dc.type | Article | |
dc.contributor.department | PHARMACOLOGY | |
dc.description.doi | 10.1016/j.regpep.2004.03.003 | |
dc.description.sourcetitle | Regulatory Peptides | |
dc.description.volume | 120 | |
dc.description.issue | 1-3 | |
dc.description.page | 149-153 | |
dc.description.coden | REPPD | |
dc.identifier.isiut | 000222225600020 | |
Appears in Collections: | Staff Publications |
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