PubMed · 12553322
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Deborah Levenson. 2002-08-09. Study validates quick blood test for heart failure.. https://pubmed.ncbi.nlm.nih.gov/12553322/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
OBJECTIVE: Interest has recently focused on the use of neurohormonal markers such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) as indices of left ventricular systolic dysfunction and prognosis in heart failure. Also, peptides belonging to the interleukin-6 (IL-6) family have been shown to induce ANP and BNP secretion. We hypothesized that BNP and ANP spillover in the peripheral circulation reflects left ventricular dysfunction and IL-6 production in septic shock. DESIGN AND SETTING: Retrospective, clinical study in the medical intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: 17 patients with septic shock and 19 control subjects. INTERVENTIONS: Collection of clinical and demographic data in relation to ANP, BNP, IL-6, and soluble TNF receptors (sTNF-R-p55, sTNF-R-p75) in plasma over a period of 4 days. MEASUREMENTS AND RESULTS: In septic shock we found a significant increase in ANP (82.7+/-9.9 vs. 14.9+/-1.2 pg/ml) and BNP (12.4+/-3.6 vs. 5.5+/-0.7 pg/ml). Plasma ANP peaked together with IL-6. Peaks of ANP and IL-6 were significantly correlated (r=0.73; p<0.01). BNP was inversely correlated to cardiac index (r=-0.56; p<0.05). CONCLUSIONS: ANP and BNP increase significantly in patients with septic shock. BNP reflects left ventricular dysfunction. ANP is related to IL-6 production rather than to cardiovascular dysfunction.
Atrial natriuretic peptide (ANP) has been shown to reduce tumor necrosis factor-alpha (TNF-alpha)-induced activation of endothelial cells via inhibition of p38 mitogen-activated protein kinase (MAPK) and nuclear factor (NF)-kappaB pathways. The aim of this study was to determine whether ANP is able to inhibit TNF-alpha-induced expression of monocyte chemoattractant protein-1 (MCP-1) in endothelial cells and to elucidate the mechanisms involved. Pretreatment of human umbilical vein endothelial cells (HUVEC) with ANP significantly reduced TNF-alpha-induced expression of MCP-1 protein and mRNA. The effects of ANP were shown to be mediated via the guanylyl-cyclase (GC)-coupled A receptor. Activation of the other GC-coupled receptor (natriuretic peptide receptor-B) by the C-type natriuretic peptide as well as activation of soluble GC with S-nitroso-L-glutathione (GSNO) exerted similar effects as ANP, supporting a role for cyclic guanosine monophosphate (cGMP) in the signal transduction. Antisense experiments showed a requirement of MAPK phosphatase-1 (MKP-1) induction and therefore, inhibition of p38 MAPK in the ANP-mediated inhibition of TNF-alpha-induced expression of MCP-1. To investigate a potential interplay between TNF-alpha-induced activation of p38 MAPK and NF-kappaB, the p38 MAPK inhibitor SB203580 and a dominant-negative p38 MAPK mutant were used. The results indicated that the blockade of p38 MAPK activity leads to an increased activation of NF-kappaB and therefore, suggest a counter-regulatory action of p38 MAPK and NF-kappaB. As antisense experiments revealed a pivotal role for MKP-1 induction and therefore, p38 MAPK inhibition in ANP-mediated attenuation of MCP-1 expression, this action seems to be rather independent of NF-kappaB inhibition.
Natriuretic peptide hormones, a family of vasoactive peptides with many favourable physiological properties, have emerged as important candidates for development of diagnostic tools and therapeutic agents in cardiovascular disease. The rapid incorporation into clinical practice of bioassays to measure natriuretic peptide concentrations, and drugs that augment the biological actions of this system, show the potential for translational research to improve patient care. Here, we focus on the physiology of the natriuretic peptide system, measurement of circulating concentrations of B-type natriuretic peptide (BNP) and the N-terminal fragment of its prohormone (N-terminal BNP) to diagnose heart failure and left ventricular dysfunction, measurement of BNP and N-terminal BNP to assess prognosis in patients with cardiac abnormalities, and use of recombinant human BNP (nesiritide) and vasopeptidase inhibitors to treat heart failure.