Southwest Texas State University
The Angiotensin Receptor (AT₁) Inhibitor, Losartan, Slows Post-Natal Thickening of the Left Ventricle
Abstract
dc:description.abstractThe overall aim of this study was to test the hypothesis that a local renin angiotensin system (RAS) in the mammalian left ventricle regulates growth of heart tissue in response to pressure-overload. Upon parturition, the mammalian left ventricle (LV) experiences pressure overload to which it responds by rapid growth, becoming thicker than the right ventricle (RV) in a few days. We assessed a role for a cardiac RAS in left ventricular development by giving losartan, an angiotensin IT (AII) AT; receptor antagonist to pregnant rats. Hearts were removed from neonates, fixed and cryosections cut with litter-mates being similarly processed at 24 hour intervals. Micrographs were obtained and morphometric analyses were performed to compare wall thickness in the left and night ventricles during neonatal development. No significant difference was found between the hearts of losartan-treated neonates and non-treated neonates. Losartan, however, inhibited LV wall thickening in treated rats during the first 48 hours of development. These results implicate involvement of the LV AT, receptor. Immunohistochemical detection of angiotensinogen (AQ) in a parallel study of these hearts indicated increased levels in the LV during the first 24 post-natal hours. These results support a role for the cardiac RAS system in controlling LV wall thickness in mammalian heart.
Degree
thesis:*- Name thesis:degree_name
- Master of Science
- Level thesis:degree_level
- Masters
- Discipline thesis:degree_discipline
- Biology
- Grantor
- Southwest Texas State University
- Year dc:date.issued
- 1994
Author and committee
dc:creator, dc:contributor.*- Author dc:creator
-
- Javadi, Fariba
- Advisor dc:contributor.advisor
-
- Koke, Joseph R.
- Committee members dc:contributor.committeemember
-
- Garcia, Dana M.
- Rose, Francis L.
Subjects
dc:subject × 4Rights
- Language dc:language.iso
- en
Identifiers
dc:identifier.*- Handle dc:identifier.uri
- https://hdl.handle.net/10877/19762
- OAI identifier oai:identifier
- oai:digital.library.txst.edu:10877/19762