Article
Potential role of the tissue renin-angiotensin system in the pathophysiology of congestive heart failure.
Cardiovascular Division, University of Minnesota Hospitals, Minneapolis 55455.
The American Journal of Cardiology (impact factor:
3.37).
11/1990;
66(11):22D-30D; discussion 30D-32D.
pp.22D-30D; discussion 30D-32D
Source: PubMed
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Citations (0)
- Cited In (6)
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Article: Rationale for the use of combination angiotensin-converting enzyme inhibitor/angiotensin II receptor blocker therapy in heart failure.
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ABSTRACT: Heart failure (HF) is a major cause of morbidity and mortality in the United States. The renin-angiotensin system (RAS) plays a major role in its pathophysiology, and angiotensin-converting enzyme (ACE) inhibitors are the cornerstone of therapy. However, HF continues to progress despite this therapy, perhaps because of production of angiotensin II by alternative pathways, which lead to direct stimulation of the angiotensin II receptor. Angiotensin II receptor blocker (ARB) therapy alone or in combination with the ACE inhibitor is a promising approach to block the RAS and slow HF progression more completely. The current medical literature on the pathophysiology of HF and the use of ACE inhibitors and ARBs was extensively reviewed. Evidence from basic science, experimental animals, and clinical trials provides data on the safety and efficacy of RAS inhibition with ACE inhibitors and ARBs as monotherapy and in combination. Data from the Evaluation of Losartan in the Elderly (ELITE) II trial indicate that ARBs alone do not appear to be more effective than ACE inhibitors in HF, but studies evaluating their use in combination are currently ongoing. The addition of an ARB offers more complete angiotensin II receptor blockade of the RAS than can be obtained by ACE inhibitors alone. Combination therapy preserves the benefits of bradykinin potentiation offered by ACE inhibitors while providing potential antitrophic influences of AT(2) receptor stimulation and may play an increased role in the treatment of chronic HF in the future.American Heart Journal 10/2000; 140(3):361-6. · 4.65 Impact Factor -
Article: Animal models of cardiorenal syndrome: a review.
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ABSTRACT: The incidence of heart failure and renal failure is increasing and is associated with poor prognosis. Moreover, these conditions do often coexist and this coexistence results in worsened outcome. Various mechanisms have been proposed as an explanation of this interrelation, including changes in hemodynamics, endothelial dysfunction, inflammation, activation of renin-angiotensin-aldosterone system, and/or sympathetic nervous system. However, the exact mechanisms initializing and maintaining this interaction are still unknown. In many experimental studies on cardiac or renal dysfunction, the function of the other organ was either not addressed or the authors failed to show any decline in its function despite histological changes. There are few studies in which the dysfunction of both heart and kidney function has been described. In this review, we discuss animal models of combined cardiorenal dysfunction. We show that translation of the results from animal studies is limited, and there is a need for new and better models of the cardiorenal interaction to improve our understanding of this syndrome. Finally, we propose several requirements that a new animal model should meet to serve as a tool for studies on the cardiorenal syndrome.Heart Failure Reviews 09/2011; 17(3):411-20. · 3.20 Impact Factor -
Article: Sympathetic activation in heart failure and its treatment with beta-blockade.
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ABSTRACT: Multiple models explaining the pathogenesis of heart failure have been put forth during the past 5 decades. These models were modified as clinical evidence supported or refuted their assumptions. During the past 2 decades, heart failure models emphasized the importance of neurohormonal systems in heart failure progression. The positive impact that angiotensin-converting enzyme inhibitors have had on mortality from heart failure has bolstered the neurohormonal theory. Attention recently has turned to the sympathetic nervous system and its potential deleterious effects on the cardiovascular system in heart failure. The sympathetic nervous system can negatively impact the cardiovascular system in heart failure in several ways, including down-regulating beta1-receptors, exerting direct toxic effects on the myocardium, and contributing to myocardial remodeling and life-threatening arrhythmias. Beta-adrenergic blockers have shown promise for reducing morbidity and mortality in heart failure, but definitive reductions in mortality remain to be shown by future investigations.Archives of Internal Medicine 03/1999; 159(3):225-34. · 11.46 Impact Factor
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Keywords
Activation
acute cardiac decompensation
angiotensin II
article reviews
cardiac impairment
cardiovascular homeostasis
cardiovascular regulation
circulating renin-angiotensin system
circulatory homeostasis
compensated stage
endogenous RAS
functional tissue RAS
heart failure
homeostatic responses
pharmacologic implications
plasma RAS
plasma renin-angiotensin activity
renal tissue RAS activities
target tissues
tissue RAS