Brain Natriuretic Peptide Release Research Articles

Pharmacodynamics and Mechanism of Astragali Radix and Anemarrhenae Rhizoma in Treating Chronic Heart Failure by Inhibiting Complement Activation.

Astragali radix (AR) and anemarrhenae rhizoma (AAR) are used clinically in Chinese medicine for the treatment of chronic heart failure (CHF), but the exact therapeutic mechanism is unclear. In this study, a total of 60 male C57BL/6 mice were divided into 5 groups, namely sham, model, AR, AAR, and AR-AAR. In the sham group, the chest was opened without ligation. In the other groups, the chest was opened and the transverse aorta was ligated to construct the transverse aortic constriction model. After 8 weeks of feeding, mice were given medicines by gavage for 4 weeks. Left ventricular ejection fraction (LVEF) and left ventricular fractional shortening (LVFS) were detected by echocardiography. Heart weight index (HWI) and wheat germ agglutinin staining were used to evaluate cardiac hypertrophy. Hematoxylin-eosin staining was used to observe the pathological morphology of myocardial tissue. Masson staining was used to evaluate myocardial fibrosis. The content of serum brain natriuretic peptide (BNP) was detected by enzyme-linked immunosorbent assay kit. The content of serum immunoglobulin G (IgG) was detected by immunoturbidimetry. The mechanism of AR-AAR in the treatment of CHF was explored by proteomics. Western blot was used to detect the protein expressions of complement component 1s (C1s), complement component 9 (C9), and terminal complement complex 5b-9 (C5b-9). The results show that AR-AAR inhibits the expression of complement proteins C1s, C9, and C5b-9 by inhibiting the production of IgG antibodies from B cell activation, which further inhibits the complement activation, attenuates myocardial fibrosis, reduces HWI and cardiomyocyte cross-sectional area, improves cardiomyocyte injury, reduces serum BNP release, elevates LVEF and LVFS, improves cardiac function, and exerts myocardial protection.

Natriuretic Peptides as Biomarkers: Narrative Review and Considerations in Cardiovascular and Respiratory Dysfunctions.

Natriuretic peptides (NPs) encompass a family of structurally related hormone/paracrine factors acting through the natriuretic peptide system regulating cell proliferation, vessel tone, inflammatory processes, neurohumoral pathways, fluids, and electrolyte balance. The three most studied peptides are atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-Type natriuretic peptide (CNP). ANP and BNP are the most relevant NPs as biomarkers for the diagnosis and prognosis of heart failure and underlying cardiovascular diseases, such as cardiac valvular dysfunction, hypertension, coronary artery disease, myocardial infarction, persistent arrhythmias, and cardiomyopathies. Cardiac dysfunctions related to cardiomyocytes stretching in the atria and ventricles are primary elicitors of ANP and BNP release, respectively. ANP and BNP would serve as biomarkers for differentiating cardiac versus noncardiac causes of dyspnea and as a tool for measuring the prognosis of patients with heart failure; nevertheless, BNP has been shown with the highest predictive value, particularly related to pulmonary disorders. Plasma BNP has been reported to help differentiate cardiac from pulmonary etiologies of dyspnea in adults and neonates. Studies have shown that COVID-19 infection also increases serum levels of N-terminal pro b-type natriuretic peptide (NT-proBNP) and BNP. This narrative review assesses aspects of ANP and BNP on their physiology, and predictive values as biomarkers. We present an overview of the NPs' synthesis, structure, storage, and release, as well as receptors and physiological roles. Following, considerations focus on ANP versus BNP, comparing their relevance in settings and diseases associated with respiratory dysfunctions. Finally, we compiled data from guidelines for using BNP as a biomarker in dyspneic patients with cardiac dysfunction, including its considerations in COVID-19.

Assessment of brain natriuretic peptide and copeptin as correlates of blood pressure in chronic hypertensive pregnant women

BackgroundHypertensive disorders of pregnancy including preexisting (or chronic) hypertension are the most common complication encountered during pregnancy that contribute significantly to maternal and perinatal morbidity and mortality. Brain natriuretic peptide (BNP) and copeptin have been investigated as biomarkers in various hypertensive disorders, but studies of their clinical value in chronic hypertensive pregnant women are sparce. This study aimed to assess the levels of BNP and copeptin in chronic hypertensive pregnant women and investigate their correlation with blood pressure (BP) in chronic hypertensive pregnant women in South Western Nigeria.MethodsOne hundred and sixty consenting pregnant women in their third trimester of pregnancy, grouped into those with chronic hypertension (n = 80) and normotensive (n = 80), were recruited for this cross-sectional study. Age and clinical characteristics were obtained, and blood was aseptically drawn for BNP and copeptin measurement using enzyme-linked immunosorbent assay. Data was analyzed with IBM SPSS ver. 20.0. Data was analyzed using Student t-test, chi-square, and Pearson correlation test as appropriate. Statistical significance was set at P < 0.05.ResultsThe mean systolic BP (SBP) and diastolic BP (DBP) were significantly higher in pregnant women with chronic hypertension (158.30 ± 3.51 and 105.08 ± 2.47 mmHg, respectively) compared with normotensive pregnant women (100.72 ± 3.02 and 70.29 ± 1.96 mmHg, respectively). The mean levels of BNP and copeptin were higher in pregnant women with chronic hypertension (57.26 ± 3.65 pg/mL and 12.44 ± 1.02 pmol/L, respectively) compared with normotensive pregnant women (49.85 ± 2.44 pg/mL and 10.25 ± 1.50 pmol/L, respectively) though not statistically significant. Correlations observed between SBP and DBP with levels of BNP (r = 0.204, P = 0.200; r = 0.142, P = 0.478) and copeptin (r = − 0.058, P = 0.288; r = 0.045, P = 0.907) were not statistically significant.ConclusionsThere was no association between BP and the levels of BNP and copeptin in pregnant women with chronic hypertension who were already on antihypertensive treatment, with the implication that antihypertensive treatment may modulate BNP and copeptin release despite significantly elevated BP levels.

Value of Brain Natriuretic Peptide in Diagnosis and Control of Hyperthyroid Patients

Background:Brain natriuretic peptide (BNP) is released from the ventricular myocardium as a reaction to volume expansion and pressure overload. Since the thyroid hormones stimulate the release of BNP, it can be used as an indicator of thyroid failure and also guiding in thyroid control .So; this study was designed to assess the value of measuring serum BNP as a marker for diagnosis and follow up of patients with subclinical and overt hyperthyroidism. Patients and Methods: This is a prospective cohort study for patients with hyperthyroidism. Patients have been enrolled from Endocrinology Outpatient Clinic at Zagazig University Hospitals in the period from December 2018 to October 2020.Results: patients were divided into two major groups, overt hyperthyroidism (group 1) and subclinical hyperthyroidism (group 2).In all cases BNP level over 100 ng/l .Median for BNP in group (1) 671.89 and the median BNP in group (2 ) 318.19 .We noticed a significant elevation of BNP levels in group (1) than group (2) ( p =

Sodium tanshinone IIA sulfonate prevents radiation-induced damage in primary rat cardiac fibroblasts.

This study investigated the effects of X-ray irradiation on primary rat cardiac fibroblasts (CFs) and its potential mechanism, as well as whether sodium tanshinone IIA sulfonate (STS) has protective effect on CFs and its possible mechanism. Our data demonstrated that X-rays inhibited cell growth and increased oxidative stress in CFs, and STS mitigated X-ray-induced injury. Enzyme-linked immuno-sorbent assay showed that X-rays increased the levels of secreted angiotensin II (Ang II) and brain natriuretic peptide (BNP). STS inhibited the X-ray-induced increases in Ang II and BNP release. Apoptosis and cell cycle of CFs were analyzed using flow cytometry. X-rays induced apoptosis in CFs, whereas STS inhibited apoptosis in CFs after X-ray irradiation. X-rays induced S-phase cell cycle arrest in CFs, which could be reversed by STS. X-rays increased the expression of phosphorylated-P38/P38, cleaved caspase-3 and caspase-3 as well as decreased the expression of phosphorylated extracellular signal-regulated kinase 1/2 (ERK 1/2)/ERK 1/2 and B cell lymphoma 2 (Bcl-2)/Bcl-2 associated X protein (BAX) in CFs, as shown by Western blotting. STS mitigated the X-ray radiation-induced expression changes of these proteins. In conclusion, our results demonstrated that STS may potentially be developed as a medical countermeasure to mitigate radiation-induced cardiac damage.

Inhibiting SLC26A4 reverses cardiac hypertrophy in H9C2 cells and in rats.

BackgroundIt has been confirmed that mutations in solute carrier family 26 member 4 (SLC26A4) contribute to pendred syndrome. However, the role of SLC26A4 in cardiac hypertrophy and the signaling pathways remain unclear.MethodsCardiomyocytes were treated by 200 µM phenylephrine (PE) to induce cardiac hypertrophy. Also, the expression of SLC26A4, GSK3, cardiac hypertrophy markers including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) was detected through real-time quantitative polymerase chain reaction (RT-qPCR). Flow cytometry assay was used to test the apoptosis of PE-induced cardiomyocytes transfected by small interfere RNA (siRNA)-SLC26A4. Furthermore, we detected the expression of autophagy-related markers including light chain 3 (LC3) and P62. Finally, we established a rat model of abdominal aortic constriction (AAC)-induced cardiac hypertrophy in vivo.ResultsRT-qPCR results showed that the mRNA expression of SLC26A4 was significantly up-regulated in PE-induced cardiac hypertrophy. After inhibiting SLC26A4, the release of ANP and BNP was significantly decreased and GSK3β was elevated in vivo and in vitro. Furthermore, inhibiting SLC26A4 promoted apoptosis of cardiac hypertrophy cells. In addition, LC3 was down-regulated and P62 was enhanced after transfection of siRNA-SLC26A4.ConclusionOur findings revealed that SLC26A4 increases cardiac hypertrophy, and inhibiting SLC26A4 could decrease the release of ANP/BNP and promote the expression of GSK-3β in vitro and in vivo. Moreover, SLC26A4 silencing inhibits autophagy of cardiomyocytes and induces apoptosis of cardiomyocytes. Therefore, SLC26A4 possesses potential value to be a therapeutic target of cardiac hypertrophy, and our study provides new insights into the mechanisms of cardiac hypertrophy.

Early Detection of Localized Immunity in Experimental Autoimmune Myocarditis Using [99mTc]Fucoidan SPECT.

The aim of the study was to evaluate the ability of technetium-99m-fucoidan ([99mTc]fucoidan), a molecular imaging agent specific for selectins, in the assessment of early localized immunity in a rat model of experimental autoimmune myocarditis (EAM). EAM was induced in Lewis rats and troponin T; brain natriuretic peptide (BNP) and anti-myosin antibodies were measured in plasma. Separately, [99mTc]fucoidan single-photon emission computed tomography (SPECT)/x-ray computed tomography (CT) was performed in the very early phase of myocarditis at 10, 15, and 21days after immunization. Then, hearts were collected and used for autoradiography, well counting, histology, and flow cytometry analysis. The EAM acute phase is characterized by extensive myocardial necrosis, release of troponin and BNP, and pericardial effusion. [99mTc]Fucoidan uptake was significantly increased in EAM compared with controls starting from D15. There was a close relationship between uptake of the tracer and myocardial content in CD45+, CD8+, CD11b+, and CD31+ cells. [99mTc]Fucoidan SPECT/CT accurately diagnosed the autoimmune attack in the early steps of EAM and could be used to monitor disease evolution and therapy efficiency.

High glucose induced calcium overload via impairment of SERCA/PLN pathway and mitochondrial dysfunction leads to oxidative stress in H9c2 cells and amelioration with ferulic acid.

Oxidative stress and associated complications are the major pathological concerns of diabetic cardiomyopathy (DC). We aim to elucidate the mechanisms by which high glucose (HG) induced alteration in calcium homeostasis and evaluation of the beneficial effect of two concentrations (10 and 25 μm) of ferulic acid (FA). HG was induced in H9c2 cardiomyoblast by treating with glucose (33 mm) for 48 h, and FA was co-treated. Intracellular calcium ([Ca2+ ]i) overload was found increased significantly with HG. For elucidation of mechanism, the SERCA pathway and mitochondrial integrity (transmembrane potential and permeability transition pore) were explored. Then, we assessed oxidative stress, and cell injury with brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and lactate dehydrogenase (LDH) release. HG caused significant [Ca2+ ]i overload through downregulation of SERCA2/1, pPLN, and pPKA C-α; and upregulation of PLN and PKA C-α and alteration in the integrity of mitochondria with HG. The [Ca2+ ]i overload in turn caused oxidative stress via generation of reactive oxygen species, lipid peroxidation, and protein carbonylation. This resulted in cell injury which was evident with significant release of BNP, ANP, and LDH. FA co-treatment was effective to mitigate all pathological changes caused by HG. From the overall results, we conclude that [Ca2+ ]i overload via SERCA pathway and altered mitochondrial integrity is the main cause for oxidative stress during HG. Based on our result, we report that FA could be an attractive nutraceutical for DC.

Rosiglitazone promotes cardiac hypertrophy and alters chromatin remodeling in isolated cardiomyocytes

Rosiglitazone is an anti-diabetic agent that raised a major controversy over its cardiovascular adverse effects. There is in vivo evidence that Rosiglitazone promotes cardiac hypertrophy by PPAR−γ-independent mechanisms. However, whether Rosiglitazone directly alters hypertrophic growth in cardiac cells is unknown. Chromatin remodeling by histone post-translational modifications has emerged as critical for many cardiomyopathies. Based on these observations, this study was initiated to investigate the cardiac hypertrophic effect of Rosiglitazone in a cellular model of primary neonatal rat cardiomyocytes (NRCM). We assessed whether the drug alters cardiac hypertrophy and its relationship with histone H3 phosphorylation. Our study showed that Rosiglitazone is a mild pro-hypertrophic agent. Rosiglitazone caused a significant increase in the release of brain natriuretic peptide (BNP) into the cell media and also increased cardiomyocytes surface area and atrial natriuretic peptide (ANP) protein expression significantly. These changes correlated with increased cardiac phosphorylation of p38 MAPK and enhanced phosphorylation of H3 at serine 10 globally and at one cardiac hypertrophic gene locus. These results demonstrate that Rosiglitazone causes direct cardiac hypertrophy in NRCM and alters H3 phosphorylation status. They suggest a new mechanism of Rosiglitazone cardiotoxicity implicating chromatin remodeling secondary to H3 phosphorylation, which activate the fetal cardiac gene program.

Quantitative assay of brain natriuretic peptide in rat cardiomyocytes in the early postreperfusion period

We studied the intensities of accumulation and secretion of brain natriuretic peptide (BNP) in the early postreperfusion period, i.e., 5 min and 1 h after the start of reperfusion in the myocardium of the right atrium of rats. Total ischemia was modeled using Korpachev’s method. Immunocytochemical detection of peptide distribution in secretory cardiomyocytes was performed in ultrathin sections using polyclonal antibodies to BNP. The immunoreactive granules of A and B types were counted in optical fields of 38 × 38 µm2 using a transmission electron microscope. Five minutes after the start of reperfusion, the number of BNPcontaining secretory granules was similar to that observed in the control animals. After a 1-h postreperfusion period, we observed active formation and release of BNP because the number of granules of A and B-types increased by 134 and 210%, respectively, as compared to the intact group. These data demonstrate the stimulating effects of ischemic and reperfusion factors on the processes of synthesis and secretion of BNP in this period.

Brain natriuretic peptide levels variation after left atrial appendage occlusion.

To explore the variations of brain natriuretic peptide (BNP) secretion after left atrial appendage occlusion. Left atrial appendage occlusion has been increasingly performed in the last few years, however little is known about the physiological consequences of left atrial appendage occlusion. Left atrial appendage regulates partially intravascular volume via release of brain natriuretic peptide. Brain natriuretic peptide levels have been related to increased risk of stroke in atrial fibrillation patients. Venous blood samples were obtained in consecutive patients undergoing left atrial appendage occlusion before, 24 hr after device implantation and at the first visit after discharge (45-60 days) for BNP measurement. Left atrial appendage occlusion was performed in 34 patients with non-valvular atrial fibrillation and contraindication to long-term oral anticoagulation or at high-risk of bleeding. There were no differences in BNP levels between baseline and 24 hr after device implantation. However left atrial appendage closure resulted in a significant decrease in BNP levels at the first follow-up visit (45-60 days) compared to baseline measurements (759.90 pg ml(-1) vs. 636.90 pgml(-1) , P = 0.013). Left atrial appendage occlusion modifies BNP levels. These levels decrease after left atrial appendage occlusion. The clinical consequences of these findings need to be evaluated in further studies. © 2015 Wiley Periodicals, Inc.

N-Terminal Pro-Brain Natriuretic Peptide (NT-proBNP) and Risk of Hypertension in the Atherosclerosis Risk in Communities (ARIC) Study.

Brain natriuretic peptide (BNP) is released by the heart in response to ventricular and auricular wall stress. Release of BNP is traditionally considered part of the body's protective mechanism against pressure overload by inducing vasodilatation and diuresis. More recent evidence demonstrates that BNP also promotes vessel wall stress and preliminary studies suggest that chronic increased levels may increase risk of hypertension. This study aimed to evaluate the prospective association of N-terminal BNP (NT-proBNP), a cleavage product of BNP, with risk of hypertension in the Atherosclerosis Risk in Communities cohort study. We conducted a prospective analysis of 3,798 middle-aged participants in the ARIC study without hypertension at baseline (1996-1998). Using Cox proportional hazards models, we characterized the association between NT-proBNP at baseline and newly diagnosed hypertension for a maximum of 14 years of follow-up (median = 9 years). We observed 2,113 new hypertension cases over the follow-up period. Higher baseline NT-proBNP was independently associated with an increased risk of hypertension. Adjusted hazard ratios for incident hypertension in the highest quartile compared to the lowest quartile of NT-proBNP at baseline was 1.24 (95% CI: 1.08-1.42). Each log-unit increase in NT-proBNP was associated with an 8% increased risk of hypertension (95% CI: 1.03-1.13). Persons with elevated NT-proBNP, even with normal blood pressure at baseline, were at increased risk of developing hypertension. Our results suggest that elevated circulating BNP might contribute to the development of hypertension in previously normotensive individuals.

Brain natriuretic peptide release in patients with aortic stenosis: Resting and exercise echocardiographic determinants

Resting and exercise echocardiographic determinants Christine Henri , Julien Magne , Raluca Dulgheru , Saloua Laaraibi , Damien Voilliot , Seisyou Kou , Luc Pierard ⁎, Patrizio Lancellotti a,⁎ a University of Liege Hospital, GIGA Cardiovascular Sciences, Department of Cardiology, Heart Valve Clinic, CHU Sart Tilman, Liege, Belgium b University of Montreal, Department of Medicine, Montreal Heart Institute, Canada

Circulating N-terminal brain natriuretic peptide and cardiac function in response to acute systemic hypoxia in healthy humans.

BackgroundAs it remains unclear whether hypoxia of cardiomyocytes could trigger the release of brain natriuretic peptide (BNP) in humans, we investigated whether breathing normobaric hypoxic gas mixture increases the circulating NT-proBNP in healthy male subjects.MethodsTen healthy young men (age 29 ± 5 yrs, BMI 24.7 ± 2.8 kg/m2) breathed normobaric hypoxic gas mixture (11% O2/89% N2) for one hour. Venous blood samples were obtained immediately before, during, and 2 and 24 hours after hypoxic exposure. Cardiac function and flow velocity profile in the middle left anterior descending coronary artery (LAD) were measured by Doppler echocardiography.ResultsArterial oxygen saturation decreased steadily from baseline value of 99 ± 1% after the initiation hypoxia challenge and reached steady-state level of 73 ± 6% within 20–30 minutes. Cardiac output increased from 6.0 ± 1.2 to 8.1 ± 1.6 L/min and ejection fraction from 67 ± 4% to 75 ± 6% (both p < 0.001). Peak diastolic flow velocity in the LAD increased from 0.16 ± 0.04 to 0.28 ± 0.07 m/s, while its diameter remained unchanged. In the whole study group, NT-proBNP was similar to baseline (60 ± 32 pmol/ml) at all time points. However, at 24 h, concentration of NT-proBNP was higher (34 ± 18%) in five subjects and lower (17 ± 17%), p = 0.002 between the groups) in five subjects than at baseline.ConclusionIn conclusion, there is no consistent increase in circulating NT-proBNP in response to breathing severely hypoxic normobaric gas mixture in healthy humans, a possible reason being that the oxygen flux to cardiac myocytes does not decrease because of increased coronary blood flow. However, the divergent individual responses as well as responses in different cardiac diseases warrant further investigations.

Hypoxia stimulates the release of Brain Natriuretic Peptide (BNP) from RPE cells

AbstractPurpose The natriuretic peptide system (A‐, B‐ and C‐type) has a powerful effect on systemic blood circulation (natriuresis, diuresis ans plasma shift) causing haemoconcentration causing increased oxygen carrying capapcity of blood. A high concentration of a member of the natriuretic peptide family has been found from the vitreous of patients suffering of proliferative diabetic retinopathy (PDR). The stimulus to which the natriuretic peptide system responded in PDR, however, has remained unknown. We tested the hypothesis that hypoxic conditions will increase the release of BNP (B‐type of natriuretic peptides) from human retinal pigment epithelium (RPE) cell cultureMethods Human retinal pigment epithelium cells (ARPE‐19) were exposed to hypoxia for 2h, 4h, 6h, 8h and 24h. The amount of BNP and VEGF (positive control) were measured at different time points in culture media using EIA. Hypoxia‐Inducible Factor (HIF), a protein, which is the master switch in regulating all the responses to hypoxia downstream, was measured using Western blotting.Results At 24h, the amount of BNP in culture media was significantly higher in hypoxic than in normoxic conditions. Also, the concentration of both VEGF and HIF were significantly higher in hypoxia.Conclusion Hypoxia increases the release of BNP from RPE cells and the response is mediated by HIF.The present results characterize for the first time a stimulus for the natriuretic peptide system in human retina and explain previous clinical findings. Thus, the measurement of natriuretic peptides in the vitreous may guide the treatment of the intraocular diseases in which the retina is suffering from hypoxia. Future perspectives: Natriuretic peptides regulate oxygen transport in all tissues?

Isoproterenol instigates cardiomyocyte apoptosis and heart failure via AMPK inactivation-mediated endoplasmic reticulum stress

A prolonged or excessive adrenergic activation leads to myocyte loss and heart dysfunction; however, how it contributes to heart failure remains poorly defined. Here we show that isoproterenol (ISO) induced aberrant endoplasmic reticulum (ER) stress and apoptotic cell death, which was inhibited by activating the AMP-activated protein kinase (AMPK) in vitro and in vivo. Persistent ISO stimulation suppressed the AMPK phosphorylation and function, resulting in enhanced ER stress and the subsequent cell apoptosis in cardiomyocytes in vitro and in vivo. AMPK activation decreased the aberrant ER stress, apoptosis, and brain natriuretic peptide (BNP) release in ISO-treated cardiomyocytes, which was blocked by AMPK inhibitor Compound C. Importantly, increased ER stress and apoptosis were observed in ISO-treated cardiomyocytes isolated from AMPKα2(-/-) mice. Inhibition of ER stress attenuated the apoptosis but failed to reverse AMPK inhibition in ISO-treated cardiomyocytes. Moreover, metformin administration activated AMPK and reduced both ER stress and apoptosis in ISO-induced rat heart failure in vivo. We conclude that ISO, via AMPK inactivation, causes aberrant ER stress, cardiomyocyte injury, BNP release, apoptosis, and hence heart failure in vivo, all of which are inhibited by AMPK activation.

Gastric Bypass Surgery Elevates NT-ProBNP Levels

Brain natriuretic peptide (BNP) is produced in the heart in response to stretching of the myocardium. BNP levels are negatively correlated to obesity, and in obese subjects, a reduced BNP responsiveness has been described. Diet-induced weight loss has been found to lower or to have no effect on BNP levels, whereas gastric banding and gastric bypass have reported divergent results. We studied obese patients undergoing gastric bypass (GBP) surgery during follow-up of 1year. Twenty patients, 18 women, mean 41 (SD 9.5) years old, with a mean preoperative BMI of 44.6 (SD 5.5) kg/m(2) were examined. N-terminal pro-brain natriuretic peptide (NT-ProBNP), glucose and insulin were measured preoperatively, at day 6 and months 1, 6 and 12. In 14 of the patients, samples were also taken at days 1, 2 and 4. The NT-ProBNP levels showed a marked increase during the postoperative week (from 54pg/mL preop to 359pg/mL on day 2 and fell to 155 on day 6). At 1year, NT-ProBNP was 122pg/mL (125% increase, p = 0.01). Glucose, insulin and HOMA indices decreased shortly after surgery without correlation to NT-ProBNP change. Mean BMI was reduced from 44.6 to 30.5kg/m(2) at 1year and was not related to NT-ProBNP change. The data indicate that GBP surgery rapidly alters the tone of BNP release, by a mechanism not related to weight loss or to changes in glucometabolic parameters. The GBP-induced conversion of obese subjects, from low to high NT-ProBNP responders, is likely to influence the evaluation of cardiac function in GBP operated individuals.

Circulation: Clinical Summaries

<i>Circulation:</i> Clinical Summaries

Brain natriuretic peptide release in acute myocardial infarction.

Brain natriuretic peptide (BNP) is released from ventricular myocites due to their stretching and volume overload. In heart failure there is BNP release. Aim of this study was to observe BNP release in acute myocardial infarction (AMI). We measured BNP in 75 patients with AMI. Control group (n=61) was similar by age and gender to AMI group. We found statistically significant elevation of BNP compared to controls (462.875 pg/ml vs 35.356 pg/ml, p< 0.001). Patients with severe systolic dysfunction had the highest BNP levels, while patients with the preserved systolic function had the lowest BNP levels (Group with EF< 30% BNP= 1129.036 pg/ml vs Group with EF31-40 % BNP= 690.177 pg/ml vs Group with EF 41-50% BNP= 274.396 pg/ml vs Group with EF> 51% BNP= 189.566 pg/ml, p< 0.001). We found statistically significant light positive correlation between BNP and left ventricle end-diastolic diameter (LVDd) (r= 0.246, p<0.05). and real positive correlation between BNP and peak troponin levels (r= 0.441, p < 0.05). BNP levels were higher in anteroseptal allocation of AMI compared to inferior allocation (835.80 pg/ml vs 243.03 pg/ml, p< 0.001) and in patients who were treated with heparin compared to fibrinolitic therapy (507.885 pg/ml vs 354.73 pg/ml, p< 0.05). BNP is elevated in AMI and is a quantitative biochemical marker related to the extent of infarction and the left ventricle systolic dysfunction. Besides echocardiographic calculation, elevation of BNP could be used for quick and easy determination of the left ventricle systolic dysfunction.

Hypoxia stimulates the synthesis and release of Brain Natriuretic Peptide (BNP) in RPE cells

AbstractPurpose Blood flow and oxygen availability of the retina are modulated by locally produced peptides that also can change the function of neurons. The natriuretic peptide system has been isolated and characterized in human retina and these peptides localize in retinal pigment epithelium (RPE) cells. A high concentration of natriuretic peptides has been previously measured from the vitreous of patients suffering of proliferative diabetic retinopathy (PDR). However, the stimulus to which the natriuretic peptide system responds in PDR has remained unknown. We hypothesized that hypoxic conditions will increase the synthesis and release of Brain Natriutretic peptide (BNP) from human RPE cell culture.Methods Human RPE cell were exposed to hypoxia for several hours. Samples were collected at time intervals and analyzed for BNP peptide and for BNP mRNA. A simultaneous measurement of VEGF served as a positive control.Results In hypoxic conditions RPE cells secreted statistically significant amounts of BNP.Conclusion These findings characterize for the first time a stimulus for the natriuretic peptide system in the retina and explain previous clinical findings. Thus, the measurement of natriuretic peptides from the vitreous may guide the treatment of the intraocular diseases in which the retina is suffering from hypoxia.