Adaptive and genetic alterations of the renin angiotensin system in cardiac hypertrophy and failure
Basic Research in Cardiology, Supplement, ISSN: 0175-9418, Vol: 91, Issue: 2, Page: 65-71
1996
- 11Citations
- 11Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations11
- Citation Indexes11
- 11
- CrossRef8
- Captures11
- Readers11
- 11
Article Description
The risk to suffer from cardiovascular events may be modulated, in part, by neurohormonal systems. Neurohormones such as angiotensin II or aldosterone may be activated secondary to congestive heart failure or in the course of an acute myocardial infarction. These systems, if activated, will subject the failing heart to increased hemodynamic load and, thus, further compromise cardiac function. In addition, structural changes of the heart and vessels occurring with pressure or volume overload may be amplified by the growth promoting effects of these agents. Taken together, the interaction of underlying cardiovascular disease and activated neurohormones may often determine clinical symptoms and prognosis. More recently, growing evidence suggests that the basal, genetically determined, activity of the renin angiotensin aldosterone system may relate to the development of cardiovascular disease as well. In particular, variants of the angiotensinogen and angiotensin converting enzyme genes have been associated with essential hypertension, myocardial infarction, or left ventricular hypertrophy. In this regard, the data suggest that the renin angiotensin aldosterone system may be one of the primary causes, rather than only a secondary co-factor, in the pathogenesis of these most important cardiovascular disorders. In light of the various options of pharmacological intervention, it seems important that ongoing clinical and molecular-genetic research will further define the role of the renin angiotensin system in clinical conditions or genetic risk profiles.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0029974056&origin=inward; http://dx.doi.org/10.1007/bf00795365; http://www.ncbi.nlm.nih.gov/pubmed/8957547; http://link.springer.com/10.1007/BF00795365; http://www.springerlink.com/index/pdf/10.1007/BF00795365; https://dx.doi.org/10.1007/bf00795365; https://link.springer.com/article/10.1007/BF00795365; http://www.springerlink.com/index/10.1007/BF00795365
Springer Nature
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