Please use this identifier to cite or link to this item: https://doi.org/10.1016/0024-3205(92)90067-Y
DC FieldValue
dc.titleEffect of experimentally-induced hypertension on angiotensin converting enzyme activity in the aortic endothelium and smooth muscle cum adventitia of the Sprague Dawley rat
dc.contributor.authorSim, M.K.
dc.contributor.authorChan, C.S.
dc.date.accessioned2012-04-02T07:42:16Z
dc.date.available2012-04-02T07:42:16Z
dc.date.issued1992
dc.identifier.citationSim, M.K., Chan, C.S. (1992). Effect of experimentally-induced hypertension on angiotensin converting enzyme activity in the aortic endothelium and smooth muscle cum adventitia of the Sprague Dawley rat. Life Sciences 50 (23) : 1821-1825. ScholarBank@NUS Repository. https://doi.org/10.1016/0024-3205(92)90067-Y
dc.identifier.issn00243205
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/32117
dc.description.abstractThe effect of experimentally-induced hypertension on the angiotensin converting enzyme (ACE) activity in the endothelium and smooth muscle cum adventitia of the Sprague Dawley rats was investigated. The ACE activity in both tissues of the 1-clip 2-kidney renovascular hypertensive rats and the deoxycorticosterone acetate/salt hypertensive rats were significantly higher than those of the normotensive control. These findings (i) support the suggestion that the 1-clip 2-kidney renovascular hypertensive rat represents a model of renin- and angiotensin-dependent hypertension and that the increased vascular ACE activity could play a role in the maintenance of hypertension (ii) provide new information regarding the association of increased vascular ACE activity and hypertension in the mineralocorticoid/salt treated hypertensive rats which may account for the finding by others that captopril is effective in preventing the development of hypertension in this low renin model of hypertension. On the other hand, the data also bring forth the possibility that the observed increase in vascular ACE activity could be the results of hypertension.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/0024-3205(92)90067-Y
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentPHARMACOLOGY
dc.description.doi10.1016/0024-3205(92)90067-Y
dc.description.sourcetitleLife Sciences
dc.description.volume50
dc.description.issue23
dc.description.page1821-1825
dc.description.codenLIFSA
dc.identifier.isiutA1992HT43400012
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