Discuss About The Regulating Circulatory Sympathovagal Balance?
For the present assessment, a number of articles have been referenced explaining the effects of increased plasma concentration of Angiotensin and its effect in the maintenance of the cardiovascular health. I think the article presented by Winkelmayer et al. (2006), is rather well documented, where the effect of Elastace has been compared in a wild types mouse with that of a Knockout mice for Elastase-2. This could be related to decrease in the cardiac inhibitory function of the Angiotensin-2 on the parasympathetic nervous system. Thus, MI could be associated with increased activation of RAS. Thus, heart failure has been linked with hyperactivity of RAS, which further increases the concentration of plasma levels of Angiotesnin. The Angiotensin levels need to be checked via the Angiotensin Converting Enzyme (ACE). The angiotensin-converting enzyme reduces the rate of heart activity by activating the parasympathetic system. It has been well explained via the sympathetic vagal balance, which has been disrupted in the mice suffering Myocardial infarction. In this respect, deletion of the ELA-2 gene decreased the basal heart rate of the mice. This proved that the same might be responsible for controlling the cardiac morbidities in the rats. The study helps in presentation of a comparative analysis where hyperactive concentration of Angiotensin have been seen to promote the rate of atherogenesis. This presents a debatable area where the use of ACE in the treatment of cardiovascular disease has been challenged
Becari, C., Durand, M. T., Guimaraes, A. O., Lataro, R. M., Prado, C. M., de Oliveira, M., … Salgado, H. C. (2017). Elastase-2, a Tissue Alternative Pathway for Angiotensin II Generation, Plays a Role in Circulatory Sympathovagal Balance in Mice. Frontiers in Physiology, 8, 170. https://doi.org/10.3389/fphys.2017.00170
Daugherty, A., Manning, M. W., & Cassis, L. A. (2000). Angiotensin II promotes atherosclerotic lesions and aneurysms in apolipoprotein E–deficient mice. Journal of Clinical Investigation, 105(11), 1605–1612.
Liu, C. L., Wang, Y., Liao, M., Wemmelund, H., Ren, J., Fernandes, C., ... & Zhang, J. Y. (2015). Allergic Lung Inflammation Aggravates Angiotensin II–Induced Abdominal Aortic Aneurysms in Mice. Arteriosclerosis, thrombosis, and vascular biology, ATVBAHA-115.
Ponnuswamy, P., Joffre, J., Herbin, O., Esposito, B., Laurans, L., Binder, C. J., ... & Zhang, Y. (2017). Angiotensin II synergizes with BAFF to promote atheroprotective regulatory B cells. Scientific Reports, 7.
Winkelmayer, W. C., Fischer, M. A., Schneeweiss, S., Levin, R., & Avorn, J. (2006). Angiotensin Inhibition After Myocardial Infarction: Does Drug Class Matter? Journal of General Internal Medicine, 21(12), 1242–1247. https://doi.org/10.1111/j.1525-1497.2006.00590.xZhang, X., Thatcher, S., Wu, C., Daugherty, A., & Cassis, L. A. (2015). Castration of male mice prevents the progression of established angiotensin II-induced abdominal aortic aneurysms. Journal of vascular surgery, 6
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