Comparison of aldosterone synthesis in adrenal cells, effect of various AT<sub>1</sub>receptor blockers with or without atrial natriuretic peptide

Miura, Shin-ichiro; Nakayama, Asuka; Tomita, Sayo; Matsuo, Yoshino; Suematsu, Yasunori; Saku, Keijiro

doi:10.3109/10641963.2014.987391

Cited by 18 publications

(14 citation statements)

References 18 publications

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“…192 Leptin stimulates aldosterone secretion from the adrenal cortex 193 and promotes its proinflammatory actions 194 ; in return, aldosterone can increase the synthesis of leptin. 195 In a counterregulatory manner, natriuretic peptides inhibit the synthesis of both leptin and aldosterone 196,197 ; circulating levels of leptin and natriuretic peptides are inversely related. 182,198 Circulating leptin levels are correlated with epicardial fat mass 163 and are increased in patients with HFpEF.…”

Section: Role Of Aldosterone Natriuretic Peptides and Leptin In The mentioning

confidence: 99%

Characterization of the inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease

Packer

Lam

Lund

et al. 2020

European J of Heart Fail

109

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Accumulating evidence points to the existence of an inflammatory-metabolic phenotype of heart failure with a preserved ejection fraction (HFpEF), which is characterized by biomarkers of inflammation, an expanded epicardial adipose tissue mass, microvascular endothelial dysfunction, normal-to-mildly increased left ventricular volumes and systolic blood pressures, and possibly, altered activity of adipocyte-associated inflammatory mediators. A broad range of adipogenic metabolic and systemic inflammatory disorders-e.g. obesity, diabetes and metabolic syndrome as well as rheumatoid arthritis and psoriasis-can cause this phenotype, independent of the presence of large vessel coronary artery disease. Interestingly, when compared with men, women are both at greater risk of and may suffer greater cardiac consequences from these systemic inflammatory and metabolic disorders. Women show disproportionate increases in left ventricular filling pressures following increases in central blood volume and have greater arterial stiffness than men. Additionally, they are particularly predisposed to epicardial and intramyocardial fat expansion and imbalances in adipocyte-associated proinflammatory mediators. The hormonal interrelationships seen in inflammatory-metabolic phenotype may explain why mineralocorticoid receptor antagonists and neprilysin inhibitors may be more effective in women than in men with HFpEF. Recognition of the inflammatory-metabolic phenotype may improve an understanding of the pathogenesis of HFpEF and enhance the ability to design clinical trials of interventions in this heterogeneous syndrome.

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Section: Role Of Aldosterone Natriuretic Peptides and Leptin In The mentioning

confidence: 99%

Characterization of the inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease

Packer

Lam

Lund

et al. 2020

European J of Heart Fail

109

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“…These reports are in agreement with our findings that olmesartan is able to attenuate cardiac remodeling. The attenuation of cardiac remodeling by treatment with olmesartan may also be attributable to its inhibition of aldosterone synthesis [ 37 ], enhancement of ACE2/Ang(1-7)/Mas axis and suppression of Nox4 expression [ 38 ], and a sustained decrease of plasma Ang II [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Olmesartan attenuates pressure-overload- or post-infarction-induced cardiac remodeling in mice

et al. 2017

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Either angiotensin converting enzyme inhibitor (ACEI) or angiotensin receptor 1 blocker (ARB) attenuates cardiac remodeling. However, the overall molecular modulation of the reversing remodeling process in response to the ACEI or ARB treatment is not yet well determined. In this study, we examined whether gene expressions are modulated by ACEI (temocapril), ARB (olmesartan) or both in a murine model with transverse aortic constriction (TAC) and confirm whether periostin is a target gene of olmesartan in mice with myocardial infarction (MI). We detected 109 genes that were significantly up-regulated in TAC mice and a majority of these were down-regulated in response to temocapril, olmesartan or their combination which significantly attenuated cardiac remodeling at one or four weeks. Real-time RT-PCR demonstrated that olmesartan, temocapril or their combination down-regulated the expression of periostin. In MI mice treated with olmesartan for 4 weeks, the left ventricular end-diastolic and systolic dimensions measured with echocardiography were lower, whereas maximum rate of rise and fall rate of LV pressure (±dp/dt max) were greater, and Azan-staining cardiac fibrotic area was smaller. Furthermore, periostin was upregulated in response to MI, whereas olmesartan blocked this upregulation. Post-MI fibrosis was smaller in periostin knockout adult mice than in wildtype mice, while glycogen synthase kinase 3β was increased and cyclin D1 was decreased in periostin knockout mice. These findings indicate that periostin is a target gene of ARB and olmesartan reverses cardiac remodeling at least partially through the downregulation of periostin.

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“…121 It was demonstrated that ANP attenuated angiotensin II-induced aldosterone synthesis in a human adrenocortical cell line (NCI-H295 R). 141…”

Section: Potential Mechanisms Underlying the Infarct-reducing And Antmentioning

confidence: 99%

The Role of Natriuretic Peptides in the Regulation of Cardiac Tolerance to Ischemia/Reperfusion and Postinfarction Heart Remodeling

Tsibulnikov

Mukhomedzyanov

Boshchenko

et al. 2020

J Cardiovasc Pharmacol Ther

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In the past 10 years, mortality from acute myocardial infarction has not decreased despite the widespread introduction of percutaneous coronary intervention. The reason for this situation is the absence in clinical practice of drugs capable of preventing reperfusion injury of the heart with high efficiency. In this regard, noteworthy natriuretic peptides (NPs) which have the infarct-limiting effect, prevent reperfusion cardiac injury, prevent adverse post-infarction remodeling of the heart. Atrial natriuretic peptide does not have the infarct-reducing effect in rats with alloxan-induced diabetes mellitus. NPs have the anti-apoptotic and anti-inflammatory effects. There is indirect evidence that NPs inhibit pyroptosis and autophagy. Published data indicate that NPs inhibit reactive oxygen species production in cardiomyocytes, aorta, heart, kidney and the endothelial cells. NPs can suppress aldosterone, angiotensin II, endothelin-1 synthesize and secretion. NPs inhibit the effects aldosterone, angiotensin II on the post-receptor level through intracellular signaling events. NPs activate guanylyl cyclase, protein kinase G and protein kinase A, and reduce phosphodiesterase 3 activity. NO-synthase and soluble guanylyl cyclase are involved in the cardioprotective effect of NPs. The cardioprotective effect of natriuretic peptides is mediated via activation of kinases (AMPK, PKC, PI3 K, ERK1/2, p70s6 k, Akt) and inhibition of glycogen synthase kinase 3β. The cardioprotective effect of NPs is mediated via sarcolemmal KATP channel and mitochondrial KATP channel opening. The cardioprotective effect of brain natriuretic peptide is mediated via MPT pore closing. The anti-fibrotic effect of NPs may be mediated through inhibition TGF-β1 expression. Natriuretic peptides can inhibit NF-κB activity and activate GATA. Hemeoxygenase-1 and peroxisome proliferator-activated receptor γ may be involved in the infarct-reducing effect of NPs. NPs exhibit the infarct-limiting effect in patients with acute myocardial infarction. NPs prevent post-infarction remodeling of the heart. To finally resolve the question of the feasibility of using NPs in AMI, a multicenter, randomized, blind, placebo-controlled study is needed to assess the effect of NPs on the mortality of patients after AMI.

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Comparison of aldosterone synthesis in adrenal cells, effect of various AT₁receptor blockers with or without atrial natriuretic peptide

Cited by 18 publications

References 18 publications

Characterization of the inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease

Characterization of the inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease

Olmesartan attenuates pressure-overload- or post-infarction-induced cardiac remodeling in mice

The Role of Natriuretic Peptides in the Regulation of Cardiac Tolerance to Ischemia/Reperfusion and Postinfarction Heart Remodeling

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Comparison of aldosterone synthesis in adrenal cells, effect of various AT1receptor blockers with or without atrial natriuretic peptide

Cited by 18 publications

References 18 publications

Characterization of the inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease

Characterization of the inflammatory‐metabolic phenotype of heart failure with a preserved ejection fraction: a hypothesis to explain influence of sex on the evolution and potential treatment of the disease

Olmesartan attenuates pressure-overload- or post-infarction-induced cardiac remodeling in mice

The Role of Natriuretic Peptides in the Regulation of Cardiac Tolerance to Ischemia/Reperfusion and Postinfarction Heart Remodeling

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Comparison of aldosterone synthesis in adrenal cells, effect of various AT₁receptor blockers with or without atrial natriuretic peptide