Angiotensin II and heart remodelling : role of ischemia, gender and pregnancy
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https://hdl.handle.net/10037/3555View/ Open
Thesis introduction (PDF)
M. B. Aljabri, T. Lund, A. C. Höper, T. V. Andreasen, S. Al-Saad, S. Lindal and K. Ytrehus: 'Gene expression, function and ischemia tolerance in male and female rat hearts after sub-toxic levels of angiotensin II', Cardiovascular Toxicology (2011), Mar;11(1):38-47, DOI: 10.1007/s12012-010-9100-0 (PDF)
Date
2011-05-26Type
Doctoral thesisDoktorgradsavhandling
Author
Aljabri, Mohammad BelalAbstract
In this thesis different factors that promote or inhibit heart remodelling induced by angiotensin II were studied. The following conclusions can be drawn:
1. The presence of elevated levels of Ang II in the perfusion buffer did not increase myocardial
injury during ischemia-reperfusion. However, the ability to protect the heart by ischemic
postconditioning was lost. This seemed to be due to blockade of ERK1/2 signalling and GSK3-β
inhibition induced by postconditioning. Elevated levels of Ang II, which is seen in untreated
cardiovascular disease and in kidney disease, could therefore contribute to limit the outcome of
the potential clinical use of postconditioning.
2. Non-compensatory (non-hypertrophic) heart remodelling was triggered by high-dose Ang II.
This leads to changes in the contractile apparatus and reduced tolerance to ischemia in the
absence of cellular hypertrophy. Increased expression of key genes involved in fibrosis was
followed by an increase in interstitial fibrosis in heart tissue, which partly explains the post
ischemic diastolic dysfunction.
3. Pregnancy did protect against the detrimental effects of Ang II since cardiac remodelling,
fibrosis and reduced vessel density were less prominent in pregnant rats.
4. Iso treatment induced heart hypertrophy in both genders, but increased fibrosis was found only in males. Unlike the situation with exposure to high concentrations of Ang II, female gender did protect against the increase in fibrosis after Iso treatment.
In summary, we can conclude that female gender and the unique female physiological status of
pregnancy protect the heart, and provide a better handling of various stress stimuli after moderate
Ang II and β-adrenergic influence. When the angiotensin II exposure reaches sub-toxic levels the protection afforded by female gender is lost.
Description
Papers number 1, 3 and 4 of this thesis are not available in Munin:
1. M. B. Aljabri , T. Lund, T. V. Andreasen and K. Ytrehus: 'Angiotensin II abates the beneficial effects of postconditioning in ERK and GSK- 3β dependent manner' (submitted paper)
3. M. B. Aljabri, N. T. Songstad, T. Lund, M. C. Serrano, T. V. Andreasen, S. Al-Saad, S. Lindal, V. Sitras, G. Acharya, K. Ytrehus: 'Pregnancy protects against antiangiogenic and fibrogenic effects of angiotensin II in rat hearts', Acta Physiologica (Oxf) (2011) Apr;201(4):445-56. Available at http://dx.doi.org/10.1111/j.1748-1716.2010.02234.x
4. M. B. Aljabri , T. Lund, S. Al-Saad, J. Benjaminsen, T. V. Andreasen and K. Ytrehus: 'Chronic isoproterenol treatment enhances extracellular fibrosis and postischemic diastolic dysfunction in male but not female rat heart' (manuscript)
1. M. B. Aljabri , T. Lund, T. V. Andreasen and K. Ytrehus: 'Angiotensin II abates the beneficial effects of postconditioning in ERK and GSK- 3β dependent manner' (submitted paper)
3. M. B. Aljabri, N. T. Songstad, T. Lund, M. C. Serrano, T. V. Andreasen, S. Al-Saad, S. Lindal, V. Sitras, G. Acharya, K. Ytrehus: 'Pregnancy protects against antiangiogenic and fibrogenic effects of angiotensin II in rat hearts', Acta Physiologica (Oxf) (2011) Apr;201(4):445-56. Available at http://dx.doi.org/10.1111/j.1748-1716.2010.02234.x
4. M. B. Aljabri , T. Lund, S. Al-Saad, J. Benjaminsen, T. V. Andreasen and K. Ytrehus: 'Chronic isoproterenol treatment enhances extracellular fibrosis and postischemic diastolic dysfunction in male but not female rat heart' (manuscript)
Publisher
Universitetet i TromsøUniversity of Tromsø
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