scholarly journals Atrial Natriuretic Peptide in Young and Elderly Children with Mild Gastroenteritis

2009 ◽  
Vol 2009 ◽  
pp. 1-4 ◽  
Author(s):  
A. Klar ◽  
E. Haver ◽  
D. Lichtstein ◽  
H. Hurvitz ◽  
T. Foah-Shauli

Objective. Atrial Natriuretic Peptide (ANP) has natriuretic and diuretic effects, synthesized and stored in the atrial cells, released in response to stretch of the atrial muscle during increase venous return. Acute gastroenteritis (AGE) causes dehydration. We intend to determine whether the decrease in venous return due to dehydration would lead to a decrease in ANP levels.Patients and Methods. This is a prospective observational controlled study. Blood collected from 30 children with AGE and ANP's levels were compared with 25 controls. ANP levels were determined by radioimmunoassay.Results. The study group was in mild dehydration. As a significant difference was found in ANP levels between children in the 3mo–3y group and older children 3y–14y. We analyzed the results according to age. No difference was found between children with AGE and control, in the 3mo–3y, ANP was 12.1±11 pg/ml versus 13.4±12 pg/ml respectively, and 3±2 versus 3.8±3 pg/ml in the 3y–14y groups, respectively.Conclusion. Dehydration due to AGE does not change the ANP's plasma levels. A weak positive correlation between sodium levels and ANP was foundr=0.29. The significant finding of our study is the difference in ANP levels related to age, in the control as well as the GE group.

1992 ◽  
Vol 263 (3) ◽  
pp. R647-R652 ◽  
Author(s):  
O. Vuolteenaho ◽  
P. Koistinen ◽  
V. Martikkala ◽  
T. Takala ◽  
J. Leppaluoto

To evaluate the role of atrial natriuretic peptide (ANP) in exercise-related cardiovascular and hormonal adjustments in hypobaric conditions, 14 young athletes performed a maximal ergometer test in a hypobaric chamber adjusted to simulate the altitudes of sea level and 3,000 m. Plasma immunoreactive ANP levels rose from 5.89 to 35.1 pmol/l at sea level and rose significantly less (P less than 0.05), from 5.36 to 22.3 pmol/l, at simulated 3,000 m. Plasma immunoreactive amino-terminal peptide of proANP (NT-proANP) levels increased to the same extent at sea level and at simulated 3,000 m (from 240 to 481 pmol/l and from 257 to 539 pmol/l, respectively). Plasma immunoreactive aldosterone increased significantly less at simulated 3,000 m (P less than 0.05), but the changes in plasma renin were similar in both conditions. Plasma immunoreactive endothelin-1 and serum erythropoietin levels remained unchanged. In conclusion, we found a blunted ANP response to maximal exercise of ANP in acute hypobaric exposure compared with that in normobaric conditions, but no significant difference in the NT-proANP responses between the two conditions. The divergence may be due to stimulation of the elimination mechanism of ANP.


1987 ◽  
Vol 252 (5) ◽  
pp. H894-H899 ◽  
Author(s):  
Y. W. Chien ◽  
E. D. Frohlich ◽  
N. C. Trippodo

To examine mechanisms by which administration of atrial natriuretic peptide (ANP) decreases venous return, we compared the hemodynamic effects of ANP (0.5 microgram X min-1 X kg-1), furosemide (FU, 10 micrograms X min-1 X kg-1), and hexamethonium (HEX, 0.5 mg X min-1 X kg-1) with those of vehicle (VE) in anesthetized rats. Compared with VE, ANP reduced mean arterial pressure (106 +/- 4 vs. 92 +/- 3 mmHg; P less than 0.05), central venous pressure (0.3 +/- 0.3 vs. -0.7 +/- 0.2 mmHg; P less than 0.01), and cardiac index (215 +/- 12 vs. 174 +/- 10 ml X min-1 X kg-1; P less than 0.05) and increased calculated resistance to venous return (32 +/- 3 vs. 42 +/- 2 mmHg X ml-1 X min X g; P less than 0.01). Mean circulatory filling pressure, distribution of blood flow between splanchnic organs and skeletal muscles, and total peripheral resistance remained unchanged. FU increased urine output similar to that of ANP, yet produced no hemodynamic changes, dissociating diuresis, and decreased cardiac output. HEX lowered arterial pressure through a reduction in total peripheral resistance without altering cardiac output or resistance to venous return. The results confirm previous findings that ANP decreases cardiac output through a reduction in venous return and suggest that this results partly from increased resistance to venous return and not from venodilation or redistribution of blood flow.


1989 ◽  
Vol 120 (4) ◽  
pp. 519-525 ◽  
Author(s):  
K. Olsson ◽  
B. E. Karlberg ◽  
L. Eriksson

Abstract. Plasma concentrations of atrial natriuretic peptide (ANP) were measured in 6 goats during pregnancy, lactation and a nonpregnant, nonlactating (= control) period before and during a rapid iv load of 0.9% NaCl. The volume of the load was 20% of blood volume. The infusions increased central venous pressure by 7 ± 1 mmHg during pregnancy and 8 ± 1 mmHg during lactation. Before infusions plasma ANP concentrations were 5.7 ± 0.7 pmol/l (control period), 10.8 ± 1.8 pmol/l (pregnancy;P< 0.05),and6.5 ± 1.5 pmol/l (lactation;NS).ANP increased significantly in all periods. Maximal values were 12.5 ± 1.5 (control period), 25.5 ± 2.3 (pregnancy; P< 0.01 vs control period, P<0.05 vs lactation), and 13.0 ± 1.6 (lactation; NS). Renal Na excretion increased similarly during pregnancy and control period, but slightly more during lactation. In 4 of the goats iv infusions of ANP (1 μg/min, 60 min) were given. The infusions caused natriuresis during the control period, but not during pregnancy and lactation, despite more than 10-fold increases of plasma ANP levels. In conclusion, our results indicate that although plasma ANP concentration rose to high levels during acute NaCl loading in pregnant goats, this effect was not important for the natriuresis. Instead, the natriuretic response to ANP appears attenuated during pregnancy, and also during lactation.


2000 ◽  
Vol 99 (4) ◽  
pp. 343-348 ◽  
Author(s):  
Kohichi TAMURA ◽  
Shinzo TAKAMORI ◽  
Hiroharu MIFUNE ◽  
Akihiro HAYASHI ◽  
Kazuo SHIROUZU

Atrial natriuretic peptide (ANP) is a cardiac hormone which affects endothelial cell function through a receptor-mediated process. Pneumonectomy is a common thoracic surgical procedure that can cause pulmonary oedema in the remaining lung. Few reports have investigated the aetiology of this complication. The aim of this study was to determine the changes in ANP concentration and expression of its receptors following pneumonectomy as a possible aetiology for postpneumonectomy pulmonary oedema (PPE). We compared plasma ANP concentrations, cGMP concentrations, and natriuretic peptide receptor (NPR)-A mRNA and NPR-C mRNA expression in rat lung 3 h after pneumonectomy (n = 5) or a sham operation (n = 5). The ANP concentrations in plasma and lung tissue in the pneumonectomy group were significantly higher than in the control group (749.5 versus 202.7 pgċml-1, P < 0.01; 33.1 versus 6.8 ngċg-1 wet tissue, P < 0.01 respectively). The level of ANP mRNA expression in the pneumonectomy group was significantly higher than in the control group (1.44 versus 0.41 relative ANP mRNA expression, P < 0.05). The concentration of cGMP and the level of NPR-A mRNA expression were not significantly different between the pneumonectomy and control groups. The level of NPR-C mRNA expression in the pneumonectomy group was significantly higher than in the control group (4.17 versus 2.19 relative NPR-C mRNA expression, P < 0.01). These findings suggest that changes in pulmonary ANP and NPR-C expression may contribute to the development of PPE in the remaining lung in the acute phase following pneumonectomy.


1997 ◽  
Vol 8 (6) ◽  
pp. 901-905
Author(s):  
X J Zhou ◽  
D Pandian ◽  
X Q Wang ◽  
N D Vaziri

Regular administration of recombinant erythropoietin (EPO) in patients with chronic renal failure (CRF) is frequently complicated by a rise in arterial blood pressure. Clinical studies intended to discern the possible role of endothelin (ET) in the pathogenesis of EPO-induced hypertension have produced contradictory results. Given the limitations of the clinical studies, this placebo-controlled study was carried out in CRF (5/6 nephrectomized) rats treated with either EPO, 150 U/kg intraperitoneally, or the vehicle alone twice weekly for 6 wk. Plasma ET was measured at baseline, and weeks 2, 4, and 6. In addition, plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined at the conclusion of the study period. As expected, blood pressure rose markedly after 1 wk of EPO therapy as compared with the placebo therapy. However, there was no significant difference in plasma ET levels between the EPO- and placebo-treated groups during the study period. Likewise, EPO therapy had no effect on plasma ANP level but depressed plasma AVP concentration. Thus, this placebo-controlled animal study revealed that EPO therapy markedly raised arterial blood pressure but had no effect on plasma ET in the CRF rats. This observation suggests that EPO-induced hypertension in this model is not mediated by an increased circulating ET level. However, the possible effect, if any, of EPO on local vascular tissue ET level is uncertain and awaits further investigation.


1995 ◽  
Vol 78 (1) ◽  
pp. 217-224 ◽  
Author(s):  
K. Nagashima ◽  
H. Nose ◽  
T. Yoshida ◽  
T. Kawabata ◽  
Y. Oda ◽  
...  

To assess the relationship between atrial natriuretic peptide (ANP) and the reduction in plasma volume (PV) during exercise, we measured changes in PV and ANP in seven male volunteers during treadmill exercise in air (AE) and with water immersion (WE) together with time control studies of rest in air and in water. Blood samples were collected from a catheter in the antecubital vein at exercise intensities of 32, 49, 65, and 78% of peak oxygen consumption (VO2). Plasma ANP in AE increased significantly from the resting value [15 +/- 1 (SE) pg/ml] only at 78% of peak VO2 (29 +/- 5 pg/ml), whereas ANP in WE increased significantly at exercise levels of > 49% of peak VO2 and reached 68 +/- 9 pg/ml at 78% of peak VO2. Although PV in AE and WE decreased significantly with VO2 of > 49% of peak VO2 (P < 0.01), the decrease from the resting value in WE was significantly greater than that in AE of > 65% of peak VO2 (P < 0.01) and the decreases at 78% of peak VO2 were -9.7 +/- 0.8 and -6.1 +/- 1.7%, respectively. The difference in the decrease in PV between AE and WE at corresponding VO2 correlated strongly with that in the increase in ANP (r = -0.97; P < 0.01). These results are consistent with the hypothesis that ANP may be involved in the fluid shift from the intra- to extravascular space during exercise.


2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Ümit Beden ◽  
Sümeyra Kaya ◽  
Volkan Yeter ◽  
Dilek Erkan

Purpose. To compare the contrast sensitivity levels of thyroid associated ophthalmopathy (TAO) patients without obvious optic neuropathy with those of healthy people.Methods. Forty eyes of 20 TAO patients without dysthyroid optic neuropathy and 40 eyes of 20 healthy subjects were evaluated in this prospective case-controlled study. The contrast sensitivity functions (CSFs) of all subjects were measured by the functional acuity contrast test (FACT) in five frequencies which were 1,5 cpd (A), 3 cpd (B), 6 cpd (C), 12 cpd (D), and 18 cpd (E). Results were compared for both groups, and a correlation of CSF with Hertel and clinical activity scores was assessed.Results. There was no statistically significant difference between TAO patients and control groups for age and sex. TAO patients had lower levels than the control group in all the frequencies of CSFs (P<0.05) and the difference in contrast sensitivity functions between the groups seems to be more significant in higher frequencies (B, C, D, and E) (P<0.001).Conclusions. TAO patients without DON can have contrast sensitivity loss and this would probably imply subtle optic nerve dysfunction in early disease phase.


2004 ◽  
Vol 14 (5) ◽  
pp. 498-505 ◽  
Author(s):  
Bamini Gopinath ◽  
Ronald J. Trent ◽  
Bing Yu

Neonatal cardiac hypertrophy associated with diabetic pregnancy is transient and regresses naturally, but is associated with increased morbidity and mortality.This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, α- and β-myosin heavy chain, and cardiac and skeletal α-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes.In the hypertrophied left ventricle of neonates from diabetic mothers, the levels of mRNA from all the above genes except skeletal α-actin were increased by between 1.8- and 12-fold compared with the controls at birth (p < 0.05). In the first 28 days, the level of mRNA for α-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and β-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate. No significant difference between the two groups of neonates was observed in all 5 genes after 1 month, indicating complete regression.Expression of 5 cardiac genes in the neonatal cardiac hypertrophy was characterised in both hypertrophic and regressive phases. Hypertrophic regression provides a unique model for the testing of new drugs or genetic modifying factors in cardiac hypertrophy.


1989 ◽  
Vol 67 (4) ◽  
pp. 326-330 ◽  
Author(s):  
Yasuaki Kawai ◽  
Toshio Ohhashi

Regional differences in responses of isolated monkey arteries and veins to atrial natriuretic peptide were investigated by recording isometric tension. Addition of atrial natriuretic peptide (4 × 10−12 to 4 × 10−8 M) produced a concentration-dependent relaxation in isolated monkey arteries and veins. No significant difference was observed between the responses to rat and human atrial natriuretic peptides. A marked heterogeneity in responses to rat atrial natriuretic peptide, however, was observed in arterial preparations. The decreasing order of the response was as follows: renal > pulmonary > femoral = mesenteric > coronary > middle cerebral > basilar arteries. A heterogeneity in the relaxation produced by atrial natriuretic peptide was also observed in monkey veins. The decreasing order of the response was as follows: pulmonary > mesenteric = portal > femoral > renal = inferior caval veins. On the other hand, 10−5 M sodium nitroprusside caused a maximal relaxation in all monkey arteries and veins used. In the middle cerebral, basilar, and coronary arteries, the relaxant effects of rat atrial natriuretic peptide on KCl-induced contraction were significantly smaller than those on the preparations contracted by an agonist such as prostaglandin F2α. These results suggest that there exist profound regional vasorelaxant selectivities of atrial natriuretic peptide in isolated monkey arteries and veins.Key words: atrial natriuretic peptide, artery, vein, vasodilation, monkey.


1997 ◽  
Vol 273 (3) ◽  
pp. F483-F487 ◽  
Author(s):  
D. W. Irons ◽  
P. H. Baylis ◽  
T. J. Butler ◽  
J. M. Davison

To further elucidate the role of atrial natriuretic peptide (ANP) in preeclampsia, its metabolic clearance (MCRANP) was determined concomitantly with its effects on sodium excretion (UNa), glomerular filtration rate (GFR), and effective renal plasma flow (ERPF). Ten untreated preeclamptic primigravidae (PET) were studied at 29-37 wk gestation and again 4 mo postpartum (PP). Basal plasma concentration of ANP was significantly increased in PET compared with PP (14.8 +/- 1.9 vs. 4.1 +/- 0.5 pmol/l, respectively; P < 0.0001). MCRANP in PET and PP was 5.0 +/- 0.8 and 4.9 +/- 0.5 l/min [not significant (NS)], respectively. In PET, infusion of ANP produced (basal vs. ANP) a natriuresis (UNa 0.14 +/- 0.02 vs. 0.28 +/- 0.04 mmol/min, P < 0.001) and an increase in GFR (97 +/- 7 vs. 106 +/- 8 ml/min, P < 0.05), with ERPF unchanged (609 +/- 24 vs. 634 +/- 29 ml/min, NS). In PP, ANP infusion also produced a natriuresis (UNa 0.20 +/- 0.02 vs. 0.25 +/- 0.02 mmol/min, P = 0.01), no significant change in GFR (109 +/- 7 vs. 102 +/- 4 ml/min), and a significant reduction in ERPF (514 +/- 22 vs. 409 +/- 18 ml/min, P < 0.0001). Analysis of variance demonstrated a greater natriuretic effect of ANP in PET compared with PP (P < 0.05), similarly a significant difference in the effect of ANP on ERPF (P < 0.01) and GFR (P < 0.05) was seen but not on filtration fraction (P = 0.35).


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