ReviewMedizinische Klinik (Munich, Germany : 1983)1998
[The renin-angiotensin system in cardiovascular diseases].
Review in Medizinische Klinik (Munich, Germany : 1983), 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
- Serial analysis of troponin I levels in patients with ischemic and nonischemic dilated cardiomyopathy.Clinical cardiology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe renin-angiotensin system is mainly involved in several cardiovascular diseases and in the pathophysiology of heart failure. It exists as a circulating and a local system which can be differently regulated. Interventions in this system by angiotensin-converting enzyme (ACE) antagonists or angiotensin-receptor antagonists slow the progression of heart failure and result in prolongation of life expectancy and improvement of hemodynamics. MECHANISMS OF ACTION: The main underlying mechanisms are: 1. Heart failure results in activation of the renin-angiotensin system as a compensatory mechanism with elevation of circulating angiotensin II, norepinephrine and vasopressin. Antagonists of this compensatory mechanisms acutely result in improvement of the hemodynamic situation. 2. Elevated circulating and local renin-angiotensin systems cause chronic structural myocardial and vascular effects. Angiotensin-converting enzyme antagonists and angiotensin-receptor blockers modulate and partly antagonize these structural changes such as myocardial hypertrophy, myocardial fibrosis and vascular proliferative responses. Gene and receptor regulation of the system are currently not fully understood and are subject of intensive research. 3. The renin-angiotensin system is closely related to the bradykinin system and thus indirectly to nitric oxide and endothelial function. Bradykinin has multiple other effects on the hemostatic system as a well as on the myocardium and vascular system.
conclusionThese complex interactions require further evaluation. Research with specific bradykinin antagonists will give new insights into this system.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.