Are elevations of N-terminal probrain natriuretic peptide in endurance athletes after prolonged strenuous exercise due to systemic inflammatory cytokines?

2006 ◽  
Vol 152 (1) ◽  
pp. e1 ◽  
Author(s):  
Craig McLachlan ◽  
Peter Mossop
Keyword(s):  
Natriuretic Peptide ◽  
Inflammatory Cytokines ◽  
Endurance Athletes ◽  
Strenuous Exercise

Independent elevations of N-terminal pro–brain natriuretic peptide and cardiac troponins in endurance athletes after prolonged strenuous exercise

2005 ◽  
Vol 150 (6) ◽  
pp. 1128-1134 ◽  
Author(s):  
Jürgen Scharhag ◽  
Markus Herrmann ◽  
Axel Urhausen ◽  
Michaela Haschke ◽  
Wolfgang Herrmann ◽  
...  
Keyword(s):  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Endurance Athletes ◽  
Strenuous Exercise ◽  
Cardiac Troponins

Effect of exercise, hyperpnea, and bronchoconstriction on plasma atrial natriuretic peptide

1989 ◽  
Vol 67 (6) ◽  
pp. 2565-2570 ◽  
Author(s):  
I. Rubinstein ◽  
T. F. Reiss ◽  
D. G. Gardner ◽  
J. Liu ◽  
B. G. Bigby ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Airway Resistance ◽  
Peak Plasma ◽  
Minute Ventilation ◽  
Significant Rise ◽  
Strenuous Exercise ◽  
Base Line ◽  
Specific Airway Resistance ◽  
Atrial Natriuretic

To examine whether endogenous secretion of atrial natriuretic peptide (ANP) modifies the bronchomotor response to moderately strenuous exercise and, conversely, whether hyperpnea of exercise or bronchoconstriction alone modulates the release of ANP, we compared the rise in specific airway resistance and the rise in circulating immunoreactive ANP (IR-ANP) induced by a 5-min submaximal exercise and by eucapnic hyperpnea with cold dry air and exercise-matched minute ventilation in six healthy individuals and in five subjects with clinically stable asthma. As expected, the increase in specific airway resistance from base line provoked by exercise was greater in the asthmatic subjects (from 11.8 +/- 7.1 to 34.0 +/- 18.6 l.cmH2O.l-1.s-1) than in the healthy subjects (from 3.7 +/- 1.2 to 4.5 +/- 1.9 l.cmH2O.l-1.s-1). In both groups, exercise was associated with a similar and significant rise in plasma IR-ANP levels, ranging from 222 to 550% from base-line value in the healthy group and from 176 to 1,120% from base-line value in the asthmatic group. Peak plasma IR-ANP levels occurred from 3 to 15 min after completion of exercise with a return to base-line values within 60 min. Although eucapnic hyperpnea was associated with a similar increase in specific airway resistance as was exercise, it provoked an increase in circulating IR-ANP in only one subject.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Circulating Immunoreactive proANP(1-30) and proANP(31-67) in Sedentary Subjects and Athletes

2000 ◽  
Vol 46 (6) ◽  
pp. 843-847 ◽  
Author(s):  
Elio F De Palo ◽  
Wolfgang Woloszczuk ◽  
Martina Meneghetti ◽  
Carlo B De Palo ◽  
Henning B Nielsen ◽  
...  
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Physical Training ◽  
Plasma Concentrations ◽  
Endurance Athletes ◽  
Plasma Samples ◽  
Electrolyte Homeostasis ◽  
Male Subjects ◽  
Sedentary Subjects ◽  
Plasma Assay

Abstract Background: Atrial natriuretic peptide (ANP) is synthesized and stored in myocytes as prohormone(1-126), which upon release is cleaved into proANP(1-98) and α-ANP(99-126). In addition, cleavage of proANP(1-98) produces proANP(1-30), proANP(31-67), and proANP(79-98) fragments. ProANP(1-30) and proANP(31-67) have roles in fluid and electrolyte homeostasis. The aim of the present study was to develop a plasma assay for proANP(1-30) and proANP(31-67) and to compare results in trained athletes and sedentary subjects. Methods: Two competitive enzyme immunoassays were established with affinity-purified sheep antiserum against synthetic ANP fragments. The immunoreactivity (ir) of proANP(1-30) and proANP(31-67) was measured in 10-μL plasma samples without extraction in a microwell-based assay. Plasma concentrations in sedentary male subjects (n = 22) and male endurance athletes (n = 14) were examined. Results: In the assay for ir-proANP(1-30) and ir-proANP(31-67), the concentrations at 95% B/B0 were 4.7 and 14.2 pmol/L, respectively. Within-run CVs were 4–6% and 5–6%, and between-run CVs were 9% for both assays. Both assays were linear on dilution (y = 0.9945x − 0.7291 and y = 1.0001x − 3.428), and the recoveries were 102–112% and 102–106%, respectively. In the sedentary and athletic groups, the ir-proANP(1-30) concentrations were similar: 318 ± 38 pmol/L and 312 ± 25 pmol/L (mean ± SE), respectively, whereas the ir-proANP(31-67) was higher in the rowers (713 ± 81 pmol/L) than in the sedentary subjects (387 ± 71 pmol/L; P <0.005). Conclusions: The proANP fragment assays are precise (CV <10%) and exhibit nearly quantitative recovery (102–112%). Only ir-proANP(31-67) responds to physical training.

EARLY AND ALTERNATIVE MARKERS OF CHRONIC HEART FAILURE IN PATIENTS WITH DIABETES MELLITUS

2021 ◽  
Vol 5 (1) ◽  
pp. 1122-1127
Author(s):  
V. Vasilkova ◽  
◽  
T. Mokhort ◽  
L. Korotaeva ◽  
Y. Yarets ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Growth Factors ◽  
Growth Factor ◽  
Natriuretic Peptide ◽  
Inflammatory Cytokines ◽  
Tnf Alpha ◽  
Reactive Protein ◽  
Patients With Diabetes ◽  
Fgf 23 ◽  
Pro Inflammatory Cytokines

Aim: to assess the relationship of proinflammatory cytokines and chemokines with the levels of natriuretic peptides in patients with diabetes mellitus (DM). Materials and methods. A total of 155 patients (14 men and 61 women) with type 1 and type 2 diabetes, aged 34 to 84 years, were examined. All patients underwent standard clinical and laboratory examination, with an assessment of the levels of pro-inflammatory cytokines (interleukin 6 (IL-6), tumour necrosis factor alpha (TNF-alpha), chemokines (monokine induced by interferon-gamma (MIG), regulated upon activation, normal T cell expressed and presumably secreted (RANTES), growth factors (fibroblast growth factor-23 (FGF-23), vascular endothelial growth factor (VEGF-A), natriuretic peptides (B‐type natriuretic peptide (BNP), N‐terminal fragment of B‐type natriuretic peptide (proBNP). Renal function was assessed based on the levels of serum creatinine, glomerular filtration rate (GFR), which was calculated according to the CKD-EPI formula, and albuminuria, which was assessed as albumin/creatinine ratio (A/C). An echocardiographic examination was conducted according to the standard protocol with the calculation of dimensional, volume and speed characteristics. Statistical data analysis was performed using smSTATA 14.2 for Mac (2018). Results. 57% DM patients had BNP and proBNP levels exceeding the diagnostic values of BNP >35 pg/ml and/or proBNP >125 pg/ml. The levels of BNP and proBNP positively correlated with the levels of homocysteine, uric acid, IL-6, С-reactive protein (CRP), high-sensitivity C-reactive protein (hsCRP), A/С, creatinine, cystatin C, TNF-alpha, chemokines (MIG, RANTES), growth factors (FGF-23, VEGF-A) (p <0.05). According to multiple regression analysis, predictors for increased proBNP were IL-6, A/K, creatinine (ß=0.70, p<0.001, ß=3.51, p=0.01, ß=0.97, p=0.01, respectively). ROC analysis determined the highest diagnostic significance of creatinine for the prediction of increased proBNP. The significance of IL-6 proved higher than A/С (AUC-0.777). Thus, when the level of IL-6 (AUC-0.789) was 3.1 mg/ml, the sensitivity and specificity for increased proBNP concentration were 71.9% and 71.2%, respectively. Conclusion. IL-6 might be an independent predictor of increased levels of natriuretic peptide in patients with diabetes. Further study of the role of pro-inflammatory cytokines in the development of cardiovascular diseases will make it possible to finally decode the mechanisms of their pathogenesis, which will further allow us to understand their complex effect on the body and obtain information for the development of new effective and safe specific medicines.

Abstract 457: Blockade of Nuclear Factor Kappa B Reverses Renal Fibrosis in Npr1 Gene-Disrupted Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Subhankar Das ◽  
Ramu Periyasamy ◽  
Kailash N Pandey
Keyword(s):  
Natriuretic Peptide ◽  
Inflammatory Cytokines ◽  
Renal Fibrosis ◽  
Nuclear Factor Kappa B ◽  
Substantial Reduction ◽  
Pyrrolidine Dithiocarbamate ◽  
Nuclear Factor ◽  
Null Mutant ◽  
Nuclear Factor Kappa ◽  
Pro Inflammatory Cytokines

Binding of atrial natriuretic peptide (ANP) to its guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA) exerts diverse physiological effects by lowering the blood pressure and blood volume. The objective of the present study was to determine the effect of blockade of nuclear factor-kappa B, inhibitory kappa B kinase, and inhibitory kappa B alpha (NF-κB, IKK, IκBα) in the kidneys of Npr1 (coding for GC-A/NPRA) gene-disrupted mice. The disruption of Npr1 greatly stimulated the renal NF-κB binding activity by 6-fold (57.12 ± 3.35 vs 9.42 ± 0.92), IKK activity by 8-fold (56.05 ± 3.83 vs 6.85 ± 0.90), and IκBα phosphorylation by 11-fold (46.67 ± 1.32 vs 4.15 ±0.58), respectively, in the kidneys of null mutant (-/-; 0-copy) mice as compared with wild-type (+/+; 2-copy) mice. Interestingly, the expression levels of IκBα were reduced by 80% (5.35 ± 0.58 vs 31.64 ± 1.13) and pro-inflammatory cytokines and renal fibrosis were enhanced by 6- to 8-fold and 5-fold (32.58 ±2.06 vs 5.85 ± 0.91), respectively, in 0-copy mice than 2-copy mice. However, the treatment of 0-copy mice with NF-κB inhibitors, andrographolide, pyrrolidine dithiocarbamate, and etanercept showed a substantial reduction in renal fibrosis by 50% (14.09 ± 2.13, 18.01 ± 1.69, and 15.88 ± 0.70, respectively), attenuation of pro-inflammatory cytokines gene expression by 60-65%, IKK activity by 60% (25.37 ± 2.22, 22.67 ± 2.23, and 19.21 ± 2.50), and IkBα phosphorylation by 65-70% (19.68 ± 1.35, 24.67 ± 1.44, 16.62 ± 1.42), respectively. Our findings demonstrate that the disruption of Npr1 activates NF-κB activity, expression of various pro-inflammatory cytokines, and renal fibrosis in 0-copy mice. However, the treatments with NF-kB inhibitors suppress NF-kB activity and pro-inflammatory cytokines and repairs the fibrosis in the kidneys of Npr1 null mutant mice. The present results suggest that the blockade of NF-kB activity provides protective effects against the inflammatory and fibrotic responses in the kidney.

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