Karunenthiran. J (2015) Research report 2: Stress and cardiovascular diseases: More insights into a possible role of RAAS. Master's Thesis / Essay, Biology.
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Abstract
Cardiovascular diseases (CVDs) are a major cause of all deaths worldwide. Endothelial dysfunction and its initiation to atherosclerosis are key factors in the development of CVD. Stress has an important role as well in the progression of CVD, although the knowledge about the exact underlying mechanism is not complete yet. Similarly, while the role of Renin-Angiotensin-Aldosterone-System (RAAS) in cardiovascular homeostasis is well described, there is not much known about the effects of stress on endothelial dysfunction through RAAS. Therefore, the present study aimed to investigate changes in RAAS activity as a consequence of stress. To evaluate this, rats from the resident-intruder paradigm were used. Intruders, which are rats that were repeatedly exposed to a social defeat interaction were compared to control rats. The two groups of animals were housed socially (group-wise) or solitary. Several parameters and measurements, including body weight, relative organ weights, tissue ACE activity, aorta vasodilatation/-constriction responses and plasma creatinine levels and ROS production were assessed in all rats. Relative organ weights were increased in solitary housed rats with respect to socially housed animals. Analysis of tissue ACE activity showed that intruders had increased ACE activity in the heart ventricle as compared to their respective controls. Absolute contraction to a high dosage of KCl was reduced in aortic rings of the group of intruders, accompanied by lack of LNMMA-mediated constriction at baseline. Furthermore, Ang2-stimulated constriction in the presence of LNMMA was significantly smaller in the latter group. These results demonstrated a remarkable impact of social stress on RAAS activity, in particular in cardiovascular tissue. Social stress by means of social defeat enhances ACE activity locally in the heart, leading to alterations in vascular function, impaired responsiveness to Ang2 and reduced basal NO-release. These observations require further experiments to understand the exact interplay between stress, RAAS and the development of CVDs.
| Item Type: | Thesis (Master's Thesis / Essay) |
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| Degree programme: | Biology |
| Thesis type: | Master's Thesis / Essay |
| Language: | English |
| Date Deposited: | 15 Feb 2018 08:10 |
| Last Modified: | 15 Feb 2018 08:10 |
| URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/13642 |
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