Renin-Angiotensin-Aldosterone Activation in Heart Failure, Aldosterone Escape

Andrew, P.

doi:10.1378/chest.122.2.755

Cited by 11 publications

(4 citation statements)

References 5 publications

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“…19 Compensation also helps to conceal the pivotal role of low CO. 21 The misperception is compounded when, having to concede that HF is a hypervolemic state, RAAS activation is then mischaracterized as "inappropriate," 14,18,20 inviting the distorted view that HF is primarily a disorder of neurohormonal control (the "neurohormonal model") rather than of fully or partially compensated low output.…”

Section: Hf (Systolic And/or Diastolic)mentioning

confidence: 99%

Diastolic Heart Failure Demystified*

Andrew¹

2003

Chest

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Section: Hf (Systolic And/or Diastolic)mentioning

confidence: 99%

Diastolic Heart Failure Demystified*

Andrew¹

2003

Chest

Self Cite

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“…In addition, blood flow velocity was decreased and contraction time was delayed. This decrease in blood flow can result in hypoperfusion, and there have been several reports that renal hypoperfusion activates the RAA system in patients with HF [25][26][27]. Reduced cardiac output in early HF induces RAAS-activated fluid retention, which subsequently increases ventricular preload and cardiac output as a compensation method.…”

Section: Discussionmentioning

confidence: 99%

Fimasartan, an angiotensin II receptor antagonist, ameliorates an in vivo zebrafish model of heart failure

Quan

Seok

et al. 2020

Korean J Intern Med

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Background/Aims: Angiotensin II in the failing heart initially helps to maintain cardiac output and blood pressure, but ultimately accelerates its deterioration. In this study, we established a model of arrhythmia-induced heart failure (HF) in zebrafish and investigated the role of renin-angiotensin-aldosterone system (RAAS) modulation by using an angiotensin II type 1 receptor blocker, fimasartan, through the assessment of cellular and physiologic responses, morbidity, and mortality. Methods: HF was induced in zebrafish larvae by exposure to 20 μM terfenadine.Morphologic, physiologic, and functional parameters were assessed in the presence or absence of fimasartan treatment. Results: Zebrafish exposed to terfenadine showed marked dilatation of the ventricle and reduced systolic function. Treatment with terfenadine was associated with 10-fold higher expression of atrial natriuretic peptide (p < 0.001 vs. vehicle), increased p53 mRNA expression, and chromatin fragmentation in the TUNEL assay, all of which were significantly reduced by fimasartan treatment. Moreover, fimasartan improved fractional shortening (terfenadine + fimasartan 16.9% ± 3.1% vs. terfenadine + vehicle 11.4% ± 5.6%, p < 0.05) and blood flow (terfenadine + fimasartan 479.1 ± 124.1 nL/sec vs. terfenadine + vehicle 273.0 ± 109.0 nL/sec, p < 0.05). Finally, treatment with fimasartan remarkably reduced mortality (terfenadine + fimasartan 36.0% vs. terfenadine + vehicle 96.0%, p < 0.001). Conclusions: Fimasartan effectively protected against the progression of HF in zebrafish by improving hemodynamic indices, which improved survival. A reduction in apoptotic cell death and an improvement in hemodynamics may be the mechanisms behind these effects. Further human studies are warranted to evaluate the possible role of fimasartan in the treatment of HF.

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“…Balb/CJ mice treated with ANG II ϩ Salt had lower cardiac output compared with C57BL/6J mice. Interestingly, Balb/CJ had lower cardiac output even though they had higher sodium and water reabsorption, which should increase blood volume, venous return, and cardiac output (2,27). Increased fluid reabsorption is a common finding in patients with pulmonary hypertension and heart failure with preserved ejection fraction (16,28).…”

Section: Discussionmentioning

confidence: 99%

Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome

Becirovic‐Agic

Jönsson

Tveitarås

et al. 2019

American Journal of Physiology-Regulatory, Integrative and Comp

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The genetic background of a mouse strain determines its susceptibility to disease. C57BL/6J and Balb/CJ are two widely used inbred mouse strains that we found react dramatically differently to angiotensin II and high-salt diet (ANG II + Salt). Balb/CJ show increased mortality associated with anuria and edema formation while C57BL/6J develop arterial hypertension but do not decompensate and die. Clinical symptoms of heart failure in Balb/CJ mice gave the hypothesis that ANG II + Salt impairs cardiac function and induces cardiac remodeling in male Balb/CJ but not in male C57BL/6J mice. To test this hypothesis, we measured cardiac function using echocardiography before treatment and every day for 7 days during treatment with ANG II + Salt. Interestingly, pulsed wave Doppler of pulmonary artery flow indicated increased pulmonary vascular resistance and right ventricle systolic pressure in Balb/CJ mice, already 24 h after ANG II + Salt treatment was started. In addition, Balb/CJ mice showed abnormal diastolic filling indicated by reduced early and late filling and increased isovolumic relaxation time. Furthermore, Balb/CJ exhibited lower cardiac output compared with C57BL/6J even though they retained more sodium and water, as assessed using metabolic cages. Left posterior wall thickness increased during ANG II + Salt treatment but did not differ between the strains. In conclusion, ANG II + Salt treatment causes early restriction of pulmonary flow and reduced left ventricular filling and cardiac output in Balb/CJ, which results in fluid retention and peripheral edema. This makes Balb/CJ a potential model to study the adaptive capacity of the heart for identifying new disease mechanisms and drug targets.

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Renin-Angiotensin-Aldosterone Activation in Heart Failure, Aldosterone Escape

Cited by 11 publications

References 5 publications

Diastolic Heart Failure Demystified*

Diastolic Heart Failure Demystified*

Fimasartan, an angiotensin II receptor antagonist, ameliorates an in vivo zebrafish model of heart failure

Time course of decompensation after angiotensin II and high-salt diet in Balb/CJ mice suggests pulmonary hypertension-induced cardiorenal syndrome

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