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The natriuretic peptide (NP) family includes atrial (ANP), brain or B-type (BNP) and C-type NP (CNP). A huge number of experimental and clinical studies, published in the 1st decade of this century, have added further support to the hypothesis that endocrine function in the human heart is a relevant component of a complex network including endocrine, nervous and immune systems. The NP hormones constitute a well-integrated regulatory system and share a similar spectrum of biological actions, although there are some differences in biological potency between ANP, BNP and CNP. However, several important issues on this field need to be investigated further. The production, secretion and peripheral degradation pathways of both BNP and CNP should be clarified in detail. In particular, the hypothesis that the circulating plasma pool of the prohormone can function as a precursor of the active peptide hormone should be demonstrated definitively. Recent findings indicate that peripheral processing of circulating prohormones could likely be submitted to regulatory rules, which might be impaired in patients with heart failure, opening up new perspectives even in the treatment of heart failure. This hypothesis suggests a novel pharmacological target for drugs inducing and/or modulating the maturation of the prohormone into active hormone., (© 2014 S. Karger AG, Basel.)

Weaning patients from mechanical ventilation has been compared to a cardiac stress test. Weaning failure (WF) from a cardiac origin can be common in patients with limited cardiac reserve. Diuretic and vasodilator therapies are indicated for WF due to excessive preload, afterload, or myocardial ischemia. Alteration in intrathoracic pressure and lung volumes may also impact weaning process in a patient with poor cardiac function. Noninvasive ventilation decreases cardiac stress load and should be utilized in weaning patients with poor cardiac reserves. In fact, positive pressure therapy is now the standard of care for treating a patient with acute pulmonary edema and to decrease afterload (Frazier et al. Biol Res Nurs 2000; 1(4): 253-264; Pinsky MR. Chest 2005; 128(5 Suppl 2): 592S-597S.). Recently, biomarkers and echocardiography have been utilized to assess weaning success during spontaneous breathing trials. In this article, we describe the physiological alterations in cardiac and pulmonary systems during the weaning process and its impact on weaning outcome.

B-type natriuretic peptide (BNP) is a plasma marker of left ventricular dysfunction and cardiac volume overload. Currently it is mainly used in the cardiovascular field. BNP is an intrinsic regulator of the embryonic stem cell proliferation, and the reduction in BNP can increase the apoptosis rate. The epitope of N terminal pro-brain natriuretic peptide-BNP is most stable. BNP1-32 has the strongest biological activity but with lower plasma level in heart failure patients. The plasma BNP level plays an important role in the diagnosis, prognosis, hospital admission and mortality of heart failure, and can be used as a monitoring indicator in the treatment of heart failure. The deficiency of corin enzyme in patients with heart failure can cause the increase of cracking pro-BNP. BNP can also provide diagnostic and prognostic information for other populations and diseases. Genetic studies on BNP and its receptors also provide important information. Nesiritide, neutral endopeptidase inhibitors, and vasopeptidase inhibitors of the natriuretic peptide synthesis have been used for the treatment of cardiovascular disorders. However, more reliable and accurate approaches for detecting BNP and N terminal pro-brain natriuretic peptide-BNP require further investigations.

Background: B-type natriuretic peptide (BNP) is released in response to extracellular volume and blood pressure (BP) overload and is a risk factor for cardiovascular diseases (CVD). BNP is increased in dialyzed patients (HDpts). The aim of this study was to evaluate the relationships between BNP and renin, aldosterone and blood volume reduction rate (BV/WL), with the presence of CVD and mortality., Methods: Fifty-one HDpts aged 70 ± 14 years were enrolled. BP, BV/WL, BNP, aldosterone, renin, C-reactive protein (CRP), troponin I and routine biochemistry were measured. According to the predialytic plasma BNP levels, the patients were divided into group A with higher BNP and group B with lower BNP than the median value of 330 pg/mL. Follow-up was 1 year., Results: After HD, plasma BNP (449.6 ± 582.2 pg/mL vs. 264.1 ± 269.8 pg/mL, p=0.0008) and aldosterone (421.8 ± 573.4 pg/mL vs. 265.1 ± 566.2 pg/mL, p=0.0003) decreased, but not rennin. BNP decreased more after hemodiafiltration than after standard HD (-55.1% ± 28.5% vs. -26.5% ± 19.5%, p=0.002). Patients in group A exhibited more diabetes (58% vs. 28%, p=0.03), ischemic heart disease (42% vs. 16%, p=0.04), left ventricular hypertrophy (88.8% vs. 33.3%, p<0.001), elevated levels of troponin I, CRP (50% vs. 24%, p=0.05), and low BV/BWL in a lower percentage (8% vs. 32%, p=0.03). After 11.2 ± 3.5 months, 8 patients (33.3%) had died in group A and 2 (8%) in group B (p=0.02)., Conclusion: This study demonstrates that BNP is high in HDpts and decreases after HD. It is correlated with a good capacity for plasma refilling, with diabetes, CVD and short-term mortality risk.

Aims: N-terminal pro-BNP (NtBNP) has attracted attention as a biomarker for heart failure. The aims of our study are (a) to characterize the role of NtBNP as a biological marker in the setting of alcoholism; (b) to describe potential gender differences with respect to NtBNP; (c) to correlate NtBNP with other clinical and haemodynamic variables., Methods: We examined 83 alcohol-dependent patients according to International Classification of Disease 10th Revision (ICD-10) and Diagnostic and Statistical Manual of Mental Disorders Fourth Edition (DSM-IV; 59 males and 24 females, age: 50 ± 10.5 years) referred to the department of psychiatry for alcohol withdrawal therapy. In these patients, we determined NtBNP, markers of alcohol abuse and transthoracic echocardiography to determine systolic left ventricular ejection fraction (EF). These measurements were repeated after alcohol withdrawal., Results: At Day 1 of alcohol withdrawal, 43 patients (52%; 27 males and 16 females) had elevated NtBNP levels (394.4 ± 438.7 pg/ml) despite normal EF (64.7 ± 6.2%). After withdrawal therapy (16.6 ± 7.8 days), NtBNP decreased significantly (228.6 ± 251.2 pg/ml; P < 0.01), despite unchanged EF (65.0 ± 5.8%; P = ns). This was the case in both males and females (328.9 ± 235.5 to 216.7 ± 194.3 pg/ml; P < 0.05 vs. 492.7 ± 635.7 to 246.6 ± 327.7 pg/ml; P < 0.05). Elevated NtBNP levels were related significantly to the history of arterial hypertension (P < 0.05)., Conclusion: This study highlights the fact that NtBNP can be elevated in the setting of alcoholism. The elevation in NtBNP is unrelated to EF and is reversible after alcohol withdrawal. We suggest a subclinical detrimental effect of alcohol abuse on cardiac function.

The natriuretic peptides are a family of related hormones that play an important role in the homeostasis of cardiovascular system. Serum levels of brain natriuretic peptide have recently emerged as a marker for the diagnosis, prognosis, follow-up, and therapy of patients with heart failure (HF) and other cardiovascular diseases. Its diagnostic role is important in valvular heart diseases, such as in severe aortic stenosis and mitral regurgitation, and in acute coronary syndromes, right ventricular dysfunction, and diastolic left ventricular dysfunction. The administration of recombinant brain natriuretic peptide in patients with acute decompensated HF has been a hot topic for the current clinical practice. Its use in patients with HF has a clinically important intermediate-term benefit without an associated increase in risk. Furthermore, it seems to have an important role in improving the hemodynamic parameters in patients with pulmonary hypertension secondary to HF and in improving postoperative renal function after coronary artery bypass grafting.

Cardiac natriuretic peptide hormones, atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP), are synthesized and secreted by the heart, producing several biological effects, such as natriuresis, vasorelaxation and hypotension. During the last decade these peptides, especially BNP, have received increasing attention as potential markers of cardiovascular disease. Their measurements can be used to diagnose heart failure, including diastolic dysfunction, and using them has been shown to save money. BNP levels can enable the differentiation between dyspnoic patients secondary to ventricular dysfunction and subjects with primary respiratory disorders. Moreover, there is good evidence that natriuretic peptides may have a diagnostic role in arterial hypertension, acute coronary syndromes, pulmonary hypertension, some valvular heart disease and some disorders affecting other systems (diabetes or thyroid disorders). In this paper we discuss the clinical utility of assessment of natriuretic peptide hormones in the diagnosis of various clinical conditions and their use as pharmacological agents.

B-type natriuretic peptide (BNP) and N-terminal-pro-BNP (NTpBNP) have a major role in screening and diagnosis of cardiac disease and monitoring of the treatment response in children and adults. This review discusses the evidence underpinning the potential benefits of these natriuretic peptides in neonatology. They may serve as a useful adjunct to echocardiography in the diagnosis of patent ductus arteriosus and its response to treatment and the diagnosis of persistent pulmonary hypertension of the newborn. However, more work is needed to explore the possible roles of BNP/NTpBNP in the management of sepsis and monitoring of cardiac performance in neonates.

Natriuretic peptide type B (brain natriuretic peptide, BNP) is a neurohormone released by cardiac ventricles in response to volume and pressure load. Recent studies have demonstrated that BNP level measured in the plasma plays an important role in cardiovascular diseases especially in the diagnosis and treatment of heart failure and acute coronary syndrome. This article summarizes the physiology of the brain natriuretic peptide, diagnosis of heart failure and acute coronary syndrome and use of BNP in the treatment and determining the prognosis of cardiovascular diseases.

Thus far, five molecules comprise the natriuretic peptide family (NPF): ANP, urodilatin, BNP, CNP and DNP. Precursor hormones for ANP, BNP and CNP are encoded by a different gene. Final peptides are ligands for A, B and C receptors, acting the latter as a clearance receptor besides neutral endopeptidase (EC 24.11). cGMP acts as a second messenger. Natriuretic peptides (NP) have well-known functions such as natriuretic, antihypertensive and reduction of plasma renin-aldosterone concentrations. An antiinflammatory ANP potential and a pro-apoptotic action in rats endothelial cells of different NP have been described. Unlike adults, NP show a different distribution during ontogeny and a different pattern of excretion under different stimuli. Noncompetitive immunoassays have become more suitable than competitive ones for routine measurement of NP with recent advances in speed of measurement. BNP and pro-BNP are emerging as useful tools in diagnosis, management and prognosis of heart disease. Preliminary data support a role of NP in the therapy of congestive heart failure. Finally, potential therapeutic compounds of NP in different pathologies are updated with an important focus on vasopeptidase inhibitors. These are capable of strengthening NP and inhibiting renin-angiotensin system at the same time, as potential useful molecules in cardiovascular therapy.

Among the most exciting developments in the field of heart failure in recent times has been the rediscovery of the natriuretic peptide system and its pleuripotent effects on cardiac structure and function. This is particularly true of its natriuretic and hemodynamic effects. There has been an explosion of the knowledge base seeking to understand the wide range of homeostatic, regulatory, and counter-regulatory functions in which the natriuretic peptide system participates. Additional interest has been stimulated by advances in technology such as point-of-care and core laboratory BNP assays and the use of the recombinant B-type natriuretic peptide nesiritide as a treatment option. Despite this recent interest, the available literature lacks a comprehensive expert review of the current science and roles of natriuretic peptides for diagnostic, prognostic, screening, treatment monitoring, and therapeutic purposes. More importantly, a summary updating and guiding the clinician on most of these advances was lacking. An expert Consensus Panel with basic, methodological, and clinical expertise was convened to summarize current knowledge in these areas and the findings and consensus statements are contained herein.

The natriuretic peptides are a group of structurally related but genetically distinct peptides. Four types of natriuretic peptides have been found thus far: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), C-type natriuretic peptide (CNP) and Dendroaspis natriuretic peptide (DNP). ANP and BNP are secreted mainly from the heart and function as hormones with vasodilatory and natriuretic effects. CNP originates mainly from endothelial cells with a paracrine effect to induce vasodilation. Other effects of natriuretic peptides including negative inotropy, antimitogenic and anticoagulation have been described. Three types of natriuretic peptide receptors mediate their functions, and among them two are cGMP-coupled. Clearance of natriuretic peptides is via its clearance receptor through the action of neutral endopeptidases. Natriuretic peptides interact with other vasoactive peptides including endothelin. The putative role of natriuretic peptides in the pathophysiology of various cardiovascular diseases including congestive heart failure, hypertension, ischemic heart disease, and cardiomyopathy are discussed. Natriuretic peptide plasma levels are used for the diagnosis and therapeutic follow-up of congestive heart failure patients. Increasing the levels of natriuretic peptides by natriuretic peptide mimetics and neutral endopeptidase inhibitors may provide a new therapeutic strategy for the treatment of cardiovascular diseases such as congestive heart failure and hypertension.

The development of new antihypertensive agents is becoming even more important. We need better blood pressure control and also agents that treat hypertension as a disease of the vascular endothelium. Recently, it has been shown that blocking the renin-angiotensin system with angiotensin converting enzyme (ACE) inhibitors reduces blood pressure and decreases the incidence of vascular disease. Another peptide system, the natriuretic peptide system, has also been shown to be important in blood pressure control and volume homeostasis. Because ACE and neutral endopeptidase, the enzyme responsible for the degradation of the natriuretic peptides, are both zinc metalloproteases, new pharmaceuticals that inhibit both enzymes have been developed. The first of these, omapatrilat, has been shown to be an effective antihypertensive agent and to have great potential for treating congestive heart failure.