Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.regpep.2005.02.007
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dc.titleEffect of des-aspartate-angiotensin I on the actions of angiotensin II in the isolated renal and mesenteric vasculature of hypertensive and STZ-induced diabetic rats
dc.contributor.authorDharmani, M.
dc.contributor.authorMustafa, M.R.
dc.contributor.authorAchike, F.I.
dc.contributor.authorSim, M.K.
dc.date.accessioned2011-09-29T05:54:39Z
dc.date.available2011-09-29T05:54:39Z
dc.date.issued2005
dc.identifier.citationDharmani, M., Mustafa, M.R., Achike, F.I., Sim, M.K. (2005). Effect of des-aspartate-angiotensin I on the actions of angiotensin II in the isolated renal and mesenteric vasculature of hypertensive and STZ-induced diabetic rats. Regulatory Peptides 129 (1-3) : 213-219. ScholarBank@NUS Repository. https://doi.org/10.1016/j.regpep.2005.02.007
dc.identifier.issn01670115
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/27281
dc.description.abstractThe 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 vasculature. Compared to the WKY, the pressor response was enhanced in the SHR and reduced in the STZ-induced diabetic rat. DAA-I attenuated the angiotensin II pressor action in renal vasculature of WKY and SHR. The attenuation was observed for DAA-I concentration as low as 10-18 M and was more prominent in SHR. However, the ability of DAA-I to reduce angiotensin II response was lost in the STZ-induced diabetic kidney. Instead, enhancement of angiotensin II pressor response was seen at the lower doses of the octapeptide. The effect of DAA-I was not inhibited by PD123319, an AT2 receptor antagonist, and indomethacin, a cyclo-oxygenase inhibitor in both WKY and SHR, indicating that its action was not mediated by angiotensin AT2 receptor and prostaglandins. The pressor responses to angiotensin II in mesenteric vascular bed were also dose-dependent but smaller in magnitude compared to the renal vasculature. The responses were significantly smaller in SHR but no significant difference was observed between STZ-induced diabetic and WKY rat. Similarly, PD123319 and indomethacin had no effect on the action of DAA-I. The findings reiterate a regulatory role for DAA-I in vascular bed of the kidney and mesentery. By being active at circulating level, DAA-I subserves a physiological role. This function appears to be present in animals with diseased state of hypertension and diabetes. It is likely that DAA-I functions are modified to accommodate the ongoing vascular remodeling. © 2005 Elsevier B.V. All rights reserved.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/j.regpep.2005.02.007
dc.sourceScopus
dc.subjectAngiotensin II
dc.subjectDes-aspartate-angiotensin I
dc.subjectMesenteric
dc.subjectRenal
dc.subjectStreptozotocin
dc.subjectVasculature
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/j.regpep.2005.02.007
dc.description.sourcetitleRegulatory Peptides
dc.description.volume129
dc.description.issue1-3
dc.description.page213-219
dc.identifier.isiut000230072400028
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