The Therapeutic Effect of Natriuretic Peptides in Heart Failure; Differential Regulation of Endothelial and Inducible Nitric Oxide Synthases

Calderone, Angelino

doi:10.1007/1-4020-7960-5_14

Cited by 6 publications

(9 citation statements)

References 144 publications

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“…This differential activity of ANP has also been reported in congestive heart failure. 40 Concomitant with the increased production of NO, NHP 73-102 expression caused a decrease in activation of NFκB. This is a significant finding, because NFκB is a central mediator of airway inflammation in patients with asthma.…”

Section: Discussionmentioning

confidence: 92%

Mechanism of bronchoprotective effects of a novel natriuretic hormone peptide☆

Hellermann

Kong

Gunnarsdottir

et al. 2004

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 92%

Mechanism of bronchoprotective effects of a novel natriuretic hormone peptide☆

Hellermann

Kong

Gunnarsdottir

et al. 2004

Journal of Allergy and Clinical Immunology

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“…23 BNP was also identified in atrial cells, but its abundance is much lower than ANP. 24 Indeed, plasma BNP levels were also found to be a powerful marker of left ventricular systolic and diastolic dysfunction and left ventricular mass in patients with heart failure. Consistent with this latter premise, prognostic assessment in patients with heart failure recently identified plasma BNP as a potent mortality predictor.…”

Section: Endothelial Dysfunction In Myocardial Hypertrophymentioning

confidence: 98%

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Tang¹,

Long²,

Wang³

et al. 2010

Journal of Cardiovascular Pharmacology

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We sought to explore new strategies targeting SUR2B/Kir6.1, a subtype of adenosine triphosphate (ATP)-sensitive potassium channels (KATP), against pressure overload-induced heart failure. The effects of natakalim, a SUR2B/Kir6.1 selective channel opener, on progression of cardiac remodeling were investigated. Pressure overload-induced heart failure was induced in Wistar rats by abdominal aortic banding. The effects of natakalim (1, 3, and 9 mg·kg⁻¹·d⁻¹ for 10 weeks) on myocardial hypertrophy and heart failure, cardiac histology, vasoactive compounds, and gene expression were assessed. Ten weeks after the onset of pressure overload, natakalim treatment potently inhibited cardiac hypertrophy and prevented heart failure. Natakalim remarkably inhibited the changes of left ventricular hemodynamic parameters and reversed the increase of heart mass index, left ventricular weight index, and lung weight index. Histological examination demonstrated that there was no significant hypertrophy or fibrosis in pressure-overloaded hearts of natakalim-treated rats. Ultrastructural examination of hearts revealed well-organized myofibrils with mitochondria grouped along the periphery of longitudinally oriented fibers in rats from the natakalim group. The content of serum nitric oxide and plasma prostacyclin was increased, whereas that of plasma endothelin-1 and cardiac tissue hydroxyproline and atrial and B-type natriuretic peptide messenger RNA was downregulated in natakalim-treated rats. Natakalim at 0.01-100 µM had no effects on isolated working hearts derived from Wistar rats; however, natakalim had endothelium-dependent vasodilatory effects on the isolated tail artery helical strips precontracted with norepinephrine. These results indicate that natakalim reduces heart failure caused by pressure overloading by activating the SUR2B/Kir6.1 KATP channel subtype and protecting against endothelial dysfunction.

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“…14 During the initial chronic phase, the peptides are responsible for maintaining sodium balance in the face of cardiac dysfunction and may ameliorate endothelial dysfunction by upregulating NOS3 and downregulating NOS2. 28 In advanced congestive heart failure, which is characterized by sodium and water retention because of low cardiac output and reduced responsiveness of the kidneys to the natriuretic peptides, both animal and clinical studies have established that ANP and BNP continue to have beneficial effects. 14 …”

Section: Atrial Natriuretic Peptide Signalingmentioning

confidence: 99%

Putting the Brakes on Cardiac Hypertrophy

Booz

2005

Hypertension

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Abstract-We know a great deal about the receptors and signaling pathways in cardiomyocytes that contribute to hypertrophic growth. Although drugs that target them have proven effective in substantially reducing left ventricular hypertrophy and associated mortality, cardiovascular disease remains the leading cause of death in the West. Another approach may rest with exploiting naturally occurring regulators of maladaptive cardiac hypertrophy that have been identified in the past few years. These endogenous negative regulators can be grouped, for the most part, into those constitutively active but whose activity is decreased by hypertrophic stimulation, and those with little or no baseline activity that are activated by hypertrophic stimulation. Spanning both groups are 4 systems that converge on cyclic guanosine 3Ј, 5Ј-monophosphate (cGMP) generation, namely natriuretic peptides (ANP and BNP), kinins, nitric oxide (NO), and the angiotensin II type 2 receptor (AT 2 ). Although holding promise as a means for restricting hypertrophy, each of these signaling molecules has certain limitations that need to be overcome. What follows is an overview of research over the past 2 years, much of it published in Hypertension, which has dealt with the antihypertrophic action of this particular group of endogenous signaling molecules. Understanding the function and regulation of the antihypertrophic NO-cGMP system offers the promise of novel therapeutic strategies for treating cardiac hypertrophy and heart failure. Key Words: adrenergic antagonists Ⅲ angiotensin II Ⅲ kinins Ⅲ natriuretic peptides Ⅲ nitric oxide synthase Ⅲ statins V arious disease states that impose an additional workload on the heart, including hypertension and myocardial infarction, lead to left ventricular (LV) hypertrophy. 1 The increase in LV mass is largely caused by increased size and protein content of cardiomyocytes and was once viewed as an adaptive response for maintaining cardiac output and tissue perfusion. After more than a decade of study, however, LV hypertrophy is recognized as a maladaptive response associated with untoward events, such as cardiomyocyte fetal gene re-expression, apoptosis, and interstitial fibrosis. 1 Untreated, LV hypertrophy generally progresses to ventricular dilatation, systolic and diastolic contractile dysfunction, and heart failure. In fact, LV hypertrophy represents a well-established risk factor for cardiovascular mortality. 2 Even the premise that cardiac hypertrophy is required to preserve heart function and normalize wall stress under conditions of pressure overload is challenged by recent studies. 1,3,4 Drugs targeting receptors and signaling pathways that couple to cardiomyocyte hypertrophic growth are highly effective in reducing LV hypertrophy and associated mortality. Yet cardiovascular disease remains the leading cause of death in the West. 5 Is there another strategy that could be used to control or reverse LV hypertrophy? An answer may rest with naturally occurring regulators of cardiac hypertrophy identified...

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The Therapeutic Effect of Natriuretic Peptides in Heart Failure; Differential Regulation of Endothelial and Inducible Nitric Oxide Synthases

Cited by 6 publications

References 144 publications

Mechanism of bronchoprotective effects of a novel natriuretic hormone peptide☆

Mechanism of bronchoprotective effects of a novel natriuretic hormone peptide☆

Activation of SUR2B/Kir6.1 Subtype of Adenosine Triphosphate-sensitive Potassium Channel Improves Pressure Overload-induced Cardiac Remodeling via Protecting Endothelial Function

Putting the Brakes on Cardiac Hypertrophy

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