atrial-natriuretic-factor and Brain-Neoplasms

atrial-natriuretic-factor has been researched along with Brain-Neoplasms* in 6 studies

Other Studies

6 other study(ies) available for atrial-natriuretic-factor and Brain-Neoplasms

ArticleYear
The productions of atrial natriuretic peptide and arginine vasopressin in small cell lung cancer with brain metastases and their associations with hyponatremia.
    European review for medical and pharmacological sciences, 2017, Volume: 21, Issue:18

    Hyponatremia is one of the most frequently encountered electrolyte disorder in small cell lung cancer (SCLC) patients. It was shown that some SCLC cell lines could produce atrial natriuretic peptide (ANP) and arginine vasopressin (AVP). The aim of the study was to assess the secretion of ANP, AVP and their relative contributions to hyponatremia in SCLC patients, especially in patients with brain metastases.. In total, 194 SCLC patients including 51 patients with brain metastases were collected. The levels of ANP and AVP were measured with radioimmunoassay kits. And then their associations with serum sodium were investigated. The progression-free survival (PFS) was compared between the hyponatremia group and the normal serum sodium group.. Serum sodium was negatively correlated with the plasma levels of ANP (r=-0.171, p=0.017) and AVP (r = -0.244, p=0.001) in all SCLC patients. In the brain metastatic subgroup, there was also a negative correlation between serum sodium and ANP (r=-0.399, p=0.004), while there was no correlation between serum sodium and AVP (r=-0.232, p=0.101). The occurrence rate of hyponatremia (serum sodium values below 135 mmol/l) in patients with brain metastases (21/51, 41.18%) was higher than that in patients without brain metastases (37/143, 25.87%) (p=0.040). The progression-free survival (PFS) in the hyponatremia group was significantly shorter than that in patients of the group without hyponatremia (p=0.010). Moreover, compared with patients which regained normal serum sodium after the treatment, the PFS of patients still with hyponatremia after the treatment was significantly shorter (p=0.049).. ANP might play a leading role in the formation of hyponatremia of SCLC patients with brain metastases. Correcting hyponatremia timely and appropriately could improve SCLC patients' prognosis.

    Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Brain Neoplasms; Disease-Free Survival; Female; Humans; Hyponatremia; Male; Middle Aged; Prognosis; Radioimmunoassay; Small Cell Lung Carcinoma; Sodium; Survival Analysis

2017
Atrial natriuretic factor: is it responsible for hyponatremia and natriuresis in neurosurgery?
    Revista Brasileira de terapia intensiva, 2016, Volume: 28, Issue:2

    To evaluate the presence of hyponatremia and natriuresis and their association with atrial natriuretic factor in neurosurgery patients.. The study included 30 patients who had been submitted to intracranial tumor resection and cerebral aneurism clipping. Both plasma and urinary sodium and plasma atrial natriuretic factor were measured during the preoperative and postoperative time periods.. Hyponatremia was present in 63.33% of the patients, particularly on the first postoperative day. Natriuresis was present in 93.33% of the patients, particularly on the second postoperative day. Plasma atrial natriuretic factor was increased in 92.60% of the patients in at least one of the postoperative days; however, there was no statistically significant association between the atrial natriuretic factor and plasma sodium and between the atrial natriuretic factor and urinary sodium.. Hyponatremia and natriuresis were present in most patients after neurosurgery; however, the atrial natriuretic factor cannot be considered to be directly responsible for these alterations in neurosurgery patients. Other natriuretic factors are likely to be involved.

    Topics: Adult; Atrial Natriuretic Factor; Brain Neoplasms; Female; Humans; Hyponatremia; Intracranial Aneurysm; Male; Middle Aged; Natriuresis; Neurosurgical Procedures; Postoperative Period; Preoperative Period; Prospective Studies; Sodium

2016
Inappropriate secretion of natriuretic peptides in a patient with a cerebral tumor.
    JAMA, 1999, Jul-07, Volume: 282, Issue:1

    Topics: Atrial Natriuretic Factor; Brain Neoplasms; Diuresis; Female; Humans; Infant; Natriuresis; Natriuretic Peptide, Brain

1999
Natriuretic peptide receptors of type A in human neuroblastomas.
    Neuroendocrinology, 1999, Volume: 70, Issue:4

    Functional natriuretic peptide receptors of type A (NPR-A) were detected in the human neuroblastoma NB-OK-1, SK-N-SH and SK-N-BE, but not the SH-SY5Y, cell lines. Also, NPR-A mRNA was detected in 19 of the 25 tumor neuroblastoma samples tested in this study. Five of the eight tumor neuroblastoma samples that were assayed for atrial natriuretic peptide (ANP) binding revealed the presence of ANP-binding sites. In the human neuroblastoma NB-OK-1 cell line, [(3)H] thymidine incorporation was increased in response to ANP, decreased in response to pituitary adenylate cyclase-activating polypeptide (PACAP-27), and the stimulatory effect of ANP was inhibited by PACAP-27. Tissue transglutaminase activity was decreased by ANP and PACAP-27, and their effects were additive. However, neither cell cycle phases, cell growth, or cell apoptosis were modified by ANP or PACAP-27 treatments.

    Topics: Apoptosis; Atrial Natriuretic Factor; Brain Neoplasms; Cell Division; Child; Child, Preschool; Enzyme Activation; Female; Flow Cytometry; Gene Expression Regulation, Neoplastic; Guanylate Cyclase; Humans; Infant; Male; Neuroblastoma; Neuropeptides; Neurotransmitter Agents; Pituitary Adenylate Cyclase-Activating Polypeptide; Receptors, Atrial Natriuretic Factor; RNA, Messenger; RNA, Neoplasm; Thymidine; Transglutaminases; Tritium; Tumor Cells, Cultured

1999
Amyloid peptides are toxic via a common oxidative mechanism.
    Proceedings of the National Academy of Sciences of the United States of America, 1995, Mar-14, Volume: 92, Issue:6

    beta-Amyloid protein (A beta) is a member of a small group of proteins that accumulate as amyloid deposits in various tissues. It has recently been demonstrated that the toxicity of A beta toward some neural cells is caused by oxidative damage. Since all of the amyloid diseases are characterized by protein deposited in the antiparallel beta-sheet conformation, it was asked whether there is a common toxic mechanism. It is shown here that the protein components of other human amyloidoses, including amylin, calcitonin, and atrial natriuretic peptide, are all toxic to clonal and primary cells. The toxicity is mediated via a free radical pathway indistinguishable from that of A beta. Experiments with synthetic peptides suggest that it is the amphiphilic nature of the peptides generated by their beta structure rather than their beta structure per se that causes toxicity. These results tend to rule out the alternative that amyloid toxicity is exclusively mediated via specific cell surface receptors.

    Topics: Amino Acid Sequence; Amyloid; Amyloid beta-Peptides; Animals; Atrial Natriuretic Factor; Brain Neoplasms; Calcitonin; Cell Line; Cell Survival; Flow Cytometry; Humans; Hydrogen Peroxide; Intercellular Signaling Peptides and Proteins; Islet Amyloid Polypeptide; L-Lactate Dehydrogenase; Melitten; Molecular Sequence Data; NADH, NADPH Oxidoreductases; Oligopeptides; Onium Compounds; p-Methoxy-N-methylphenethylamine; Peptide Fragments; Peptides; Protein Structure, Secondary; Rats; Structure-Activity Relationship; Tumor Cells, Cultured; Wasp Venoms

1995
Specific binding of atrial natriuretic peptide increases cyclic GMP levels in human astrocytoma cells.
    The Journal of endocrinology, 1988, Volume: 117, Issue:2

    Specific high-affinity binding sites (dissociation constant 100 pmol/l) for atrial natriuretic peptide (ANP) have been identified in the clone D384 derived from the human astrocytoma cell line G-CCM. Unrelated peptides such as angiotensin II, vasopressin and bradykinin did not compete for these sites. Of the atrial natriuretic peptides studied, both the human and rat ANP competed equally, while peptides with either C- or N-terminal residue missing or with no internal -S-S-bond either competed less effectively or did not compete at all. Human ANP stimulated the cells to increase their intracellular level of cyclic GMP in a time- and dose-dependent manner with maximum stimulation being approached but not reached at concentrations of 1 mumol/l. These results support both the notion that ANP has an important functional role within the brain and the concept of neurotransmitter/neuromodulator communication between neurones and glia.

    Topics: Astrocytoma; Atrial Natriuretic Factor; Binding Sites; Brain Neoplasms; Cyclic GMP; Humans; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface; Tumor Cells, Cultured

1988