Effects of long-term enalapril and losartan therapy of heart failure on cardiovascular aldosterone

Xiu, Jiancheng; Wu, Peng; Guo, Zhigang; Lai, Wenyan; Zhang, Y.; Li, S.; Li, J.; Liu, Y.

doi:10.1007/bf03344039

Cited by 16 publications

(11 citation statements)

References 27 publications

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“…Aldosterone synthase (CYP11B2) is detected in the hearts of several species, including rats 9,10 and humans. 11,12 Cardiac aldosterone production has also been found in experiments demonstrating a gradient of plasma aldosterone concentrations between the anterior interventricular vein and coronary sinus in humans, 13,14 and myocardial production of aldosterone has been demonstrated in the rat. 15 Increased production of cardiac aldosterone under certain pathological conditions suggests that it could play an important role in the pathogenesis of cardiac diseases.…”

mentioning

confidence: 79%

Persistent Cardiac Aldosterone Synthesis in Angiotensin II Type 1A Receptor–Knockout Mice After Myocardial Infarction

et al. 2005

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Background-The renin-angiotensin-aldosterone system is implicated in the pathogenesis of heart failure. Pharmacological blockade of angiotensin II (Ang II)-dependent signaling is clinically effective in reducing cardiovascular events after myocardial infarction (MI) but still fails to completely prevent remodeling. The molecular basis underlying this Ang II-independent remodeling is unclear. Methods and Results-Acute MI was induced by coronary ligation in wild-type (WT) and angiotensin II type IA receptor-knockout (AT 1A -KO) mice. Left ventricular (LV) geometry, hemodynamics, and cardiac gene expression were evaluated on day 28. Severe LV remodeling and resultant cardiac dysfunction were observed in WT mice, whereas less marked, but still significant, LV remodeling and cardiac dysfunction were induced in AT 1A -KO mice. Gene expression levels of aldosterone synthase and the cardiac aldosterone content were both elevated in the MI hearts, even in AT 1A -KO mice. In AT 1A -KO mice treated with spironolactone (20 mg/kg per day), LV remodeling, cardiac dysfunction, and cardiac gene expression of collagens and natriuretic peptides were almost normalized. Conclusions-Our results indicate that genetic blockade of AT 1A signaling fails to arrest aldosterone production in cardiac tissues and that cardiac aldosterone plays a critical role in post-MI LV remodeling. The results suggest that spironolactone could be potentially effective in patients with MI, when used in combination with renin-angiotensin system blockade, by blocking the actions of aldosterone produced by Ang II-independent mechanisms. (Circulation. 2005;111:2157-2164.)

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confidence: 79%

Persistent Cardiac Aldosterone Synthesis in Angiotensin II Type 1A Receptor–Knockout Mice After Myocardial Infarction

et al. 2005

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“…For example, rats subjected to myocardial infarction showed an increase in both cardiac aldosterone synthase (CYP11B2) and aldosterone levels [24], whereas aldosterone synthase mRNA was not found in Sprague Dawley rat hearts unless the rats were subjected to chronic Ang-II infusions [25]. Others have found an all together complete lack of aldosterone synthase expression in rats [26].…”

Section: Aldosterone Productionmentioning

confidence: 99%

Cardiac Hypertrophy and Fibrosis in the Metabolic Syndrome: A Role for Aldosterone and the Mineralocorticoid Receptor

Essick

Sam

2011

International Journal of Hypertension

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Obesity and hypertension, major risk factors for the metabolic syndrome, render individuals susceptible to an increased risk of cardiovascular complications, such as adverse cardiac remodeling and heart failure. There has been much investigation into the role that an increase in the renin-angiotensin-aldosterone system (RAAS) plays in the pathogenesis of metabolic syndrome and in particular, how aldosterone mediates left ventricular hypertrophy and increased cardiac fibrosis via its interaction with the mineralocorticoid receptor (MR). Here, we review the pertinent findings that link obesity with elevated aldosterone and the development of cardiac hypertrophy and fibrosis associated with the metabolic syndrome. These studies illustrate a complex cross-talk between adipose tissue, the heart, and the adrenal cortex. Furthermore, we discuss findings from our laboratory that suggest that cardiac hypertrophy and fibrosis in the metabolic syndrome may involve cross-talk between aldosterone and adipokines (such as adiponectin).

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“…55 Similarly, in rats with experimental myocardial infarction, although plasma aldosterone production was markedly inhibited by ACEI and ARB, myocardial aldosterone concentration was increased in the group treated with ACEI and was suppressed in the ARB group. 64 A perplexing phenomenon is the increase in plasma aldosterone concentration observed during combination ACEI and ARB treatment in people. 65 In 1 study after 17 weeks of treatment, plasma aldosterone concentration was greatly decreased, but by 43 weeks plasma aldosterone concentration returned to baseline despite maximal doses of both ACEI and ARB.…”

Section: 63mentioning

confidence: 99%

The Effect of Ramipril on Left Ventricular Mass, Myocardial Fibrosis, Diastolic Function, and Plasma Neurohormones in Maine Coon Cats with Familial Hypertrophic Cardiomyopathy without Heart Failure

MacDonald

Kittleson

Larson

et al. 2006

Veterinary Internal Medicne

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Background: Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats, resulting in left ventricular (LV) hypertrophy, myocardial fibrosis, and diastolic dysfunction.Hypothesis: Ramipril will reduce LV mass, improve diastolic function, and reduce myocardial fibrosis in cats with HCM without congestive heart failure (CHF).Animals: This prospective, blinded, placebo-controlled study included 26 Maine Coon and Maine Coon cross-bred cats with familial HCM but without CHF.Methods: Cats were matched for LV mass index (LVMI) and were randomized to receive ramipril (0.5 mg/kg) or placebo q24h for 1 year, with investigators blinded. Plasma brain natriuretic peptide (BNP) concentration, plasma aldosterone concentration, Doppler tissue imaging (DTI), and systolic blood pressure were measured at baseline and every 3 months for 1 year. Cardiac magnetic resonance imaging (cMRI) was performed to quantify LV mass and myocardial fibrosis by delayed enhancement (DE) cMRI at baseline and 6 and 12 months. Plasma angiotensin-converting enzyme (ACE) activity was measured on 16 cats 1 hour after PO administration.Results: Plasma ACE activity was adequately suppressed (97%) in cats treated with ramipril. LV mass, LVMI, DTI, DE, blood pressure, plasma BNP, and plasma aldosterone were not different in cats treated with ramipril compared with placebo (P 5 .85, P 5 .94, P 5 .91, P 5 .89, P 5 .28, P 5 .18, and P 5 .25, respectively).Conclusion: Treatment of Maine Coon cats with HCM without CHF with ramipril did not change LV mass, improve diastolic function, alter DE, or alter plasma BNP or aldosterone concentrations in a relevant manner.

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Effects of long-term enalapril and losartan therapy of heart failure on cardiovascular aldosterone

Cited by 16 publications

References 27 publications

Persistent Cardiac Aldosterone Synthesis in Angiotensin II Type 1A Receptor–Knockout Mice After Myocardial Infarction

Persistent Cardiac Aldosterone Synthesis in Angiotensin II Type 1A Receptor–Knockout Mice After Myocardial Infarction

Cardiac Hypertrophy and Fibrosis in the Metabolic Syndrome: A Role for Aldosterone and the Mineralocorticoid Receptor

The Effect of Ramipril on Left Ventricular Mass, Myocardial Fibrosis, Diastolic Function, and Plasma Neurohormones in Maine Coon Cats with Familial Hypertrophic Cardiomyopathy without Heart Failure

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