Changes in atrial natriuretic peptide concentration and expression of its receptors after pneumonectomy in the rat

2000 ◽  
Vol 99 (4) ◽  
pp. 343-348 ◽  
Author(s):  
Kohichi TAMURA ◽  
Shinzo TAKAMORI ◽  
Hiroharu MIFUNE ◽  
Akihiro HAYASHI ◽  
Kazuo SHIROUZU
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Mrna Expression ◽  
Pulmonary Oedema ◽  
Natriuretic Peptide ◽  
Cell Function ◽  
Control Group ◽  
Sham Operation ◽  
Endothelial Cell Function ◽  
And Control ◽  
Atrial Natriuretic

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.

scholarly journals Therapeutic role of atrial natriuretic peptide in early treatment of traumatic hemorrhagic shock

2021 ◽  
Vol 19 ◽  
pp. 205873922110044
Author(s):  
Shou-Yin Jiang ◽  
Ye-Hua Shen ◽  
Tai-Wen Rao ◽  
Xiao-Gang Zhao
Keyword(s):  
Oxidative Stress ◽  
Atrial Natriuretic Peptide ◽  
Hemorrhagic Shock ◽  
Natriuretic Peptide ◽  
Sham Group ◽  
Control Group ◽  
Organ Protection ◽  
Traumatic Hemorrhagic Shock ◽  
And Control ◽  
Atrial Natriuretic

The biological effect of atrial natriuretic peptide (ANP) in traumatic hemorrhagic shock (THS) is unknown. This study was to evaluate whether ANP therapy can show organ protection in THS. Thirty male Sprague-Dawley rats were divided into three groups: ANP group, sham group, and control group. Pressure-controlled THS was induced in rats in ANP group and control group. ANP at a rate of 0.025 μg/kg/min was infused in ANP group during near-80 min of shock. After that, animals were resuscitated for 60 min and observed until 24 h. Hemodynamic parameters during shock and resuscitation were measured. Serum levels of ANP and lactate dehydrogenase, tissue oxidative stress and inflammatory factors, as well as liver and kidney function were determined. Tissue apoptosis was also assessed. There was no statistically significant difference between ANP group and control group in arterial pressure throughout the 150 min monitoring period. Blood urea nitrogen at 90 min and 24 h in ANP group was significantly lower than control group. Alanine transaminase and aspartate aminotransferase activity at 90 min in control group were significantly higher than that in sham group. However, hepatic enzyme activity at 90 min in ANP group was not significantly different compared with sham or control group. After 24 h, myocardial expression of caspase 3 protein in ANP group was significantly reduced compared with control group. Jejunal and hepatic Malondialdehyde was increased following ANP treatment. ANP therapy during early THS has no significant adverse effect on hemodynamics but can exert oxidative stress and certain protective effect on multiple organs. Our study may shed light on the novel therapy of THS with regard to organ protection. The mechanisms underlying the organ protection require further study.

Atrial natriuretic peptide in pregnant and lactating goats

1989 ◽  
Vol 120 (4) ◽  
pp. 519-525 ◽  
Author(s):  
K. Olsson ◽  
B. E. Karlberg ◽  
L. Eriksson
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Venous Pressure ◽  
Control Period ◽  
Plasma Concentrations ◽  
Central Venous ◽  
Lactating Goats ◽  
Pregnancy And Lactation ◽  
And Control ◽  
Atrial Natriuretic

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.

scholarly journals Atrial natriuretic peptide modulates cystic fibrosis transmembrane conductance regulator chloride channel expression in rat proximal colon and human intestinal epithelial cells

2006 ◽  
Vol 189 (1) ◽  
pp. 155-165 ◽  
Author(s):  
H J Novaira ◽  
D S Ornellas ◽  
T M Ortiga-Carvalho ◽  
X M Zhang ◽  
J Souza-Menezes ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epithelial Cells ◽  
Atrial Natriuretic Peptide ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Proximal Colon ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Cystic Fibrosis Transmembrane ◽  
Atrial Natriuretic

The cystic fibrosis transmembrane conductance regulator (CFTR) is one of the most intensively investigated Cl− channels. Different mutations in the CFTR gene cause the disease cystic fibrosis (CF). CFTR is expressed in the apical membrane of various epithelial cells including the intestine. The major organ affected in CF patients is the lung, but it also causes an important dysfunction of intestinal ion transport. The modulation of CFTR mRNA expression by atrial natriuretic peptide (ANP) was investigated in rat proximal colon and in human intestinal CaCo-2 cells by RNase protection assay and semi-quantitative reverse transcriptase PCR techniques. Groups of rats subjected to volume expansion or intravenous infusion of synthetic ANP showed respective increases of 60 and 50% of CFTR mRNA expression in proximal colon. CFTR mRNA was also increased in cells treated with ANP, reaching a maximum effect at 10−9 M ANP, probably via cGMP. ANP at 10−9 M was also able to stimulate both the CFTR promoter region (by luciferase assay) and protein expression in CaCo-2 cells (by Western blot and immunoprecipitation/phosphorylation). These results suggested the involvement of ANP, a hormone involved with extracellular volume, in the expression of CFTR in rat proximal colon and CaCo-2 intestinal cells.

scholarly journals Epigenetic Downregulation of Atrial Natriuretic Peptide but not Vasopressin mRNA Expression in Females with Eating Disorders is Related to Impulsivity

2008 ◽  
Vol 33 (11) ◽  
pp. 2605-2609 ◽  
Author(s):  
Helge Frieling ◽  
Stefan Bleich ◽  
Jeannette Otten ◽  
Konstanze D Römer ◽  
Johannes Kornhuber ◽  
...  
Keyword(s):  
Eating Disorders ◽  
Atrial Natriuretic Peptide ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Atrial Natriuretic

Hypothermic Circulatory Arrest: Renal Protection by Atrial Natriuretic Peptide

2009 ◽  
Vol 17 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Masahiro Ohno ◽  
Tadashi Omoto ◽  
Masaomi Fukuzumi ◽  
Masaya Oi ◽  
Noboru Ishikawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Circulatory Arrest ◽  
Treated Group ◽  
Hypothermic Circulatory Arrest ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Medullary Blood Flow ◽  
Atrial Natriuretic

Moderate hypothermic circulatory arrest with selective cerebral perfusion has been developed for cerebral protection during thoracic aortic surgery. However, visceral organs, particularly the kidneys, suffer greater tissue damage under moderate hypothermic circulatory arrest, and acute renal failure after hypothermic circulatory arrest is an independent risk factor for early and late mortality. This study investigated whether atrial natriuretic peptide could prevent the reduction in renal perfusion and protect renal function after moderate hypothermic circulatory arrest. Twelve pigs cooled to 30°C during cardiopulmonary bypass were randomly assigned to a peptide-treated group of 6 and a control group of 6. Moderate hypothermic circulatory arrest was induced for 60 min. Systemic arterial mean pressure and renal artery flow did not differ between groups during the study. However, renal medullary blood flow increased significantly in the peptide-treated group after hypothermic circulatory arrest. Myeloperoxidase activity was significantly reduced in the medulla of the peptide-treated group. Renal medullary ischemia after hypothermic circulatory arrest was ameliorated by atrial natriuretic peptide which increased medullary blood flow and reduced sodium reabsorption in the medulla. Atrial natriuretic peptide also reduced the release of an inflammatory marker after ischemia in renal tissue.

Response to dynamic exercise in cardiac transplant recipients: implications for control of the sodium regulatory hormone atrial natriuretic peptide

1990 ◽  
Vol 78 (2) ◽  
pp. 159-163 ◽  
Author(s):  
D. R. J. Singer ◽  
N. R. Banner ◽  
A. Cox ◽  
N. Patel ◽  
M. Burdon ◽  
...  
Keyword(s):  
Heart Rate ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Control Group ◽  
Cardiac Transplant ◽  
Cardiac Innervation ◽  
Transplant Recipients ◽  
Plasma Atrial Natriuretic Peptide ◽  
Control Subjects ◽  
Atrial Natriuretic

1. To study the importance of cardiac innervation in the regulation of atrial natriuretic peptide, plasma atrial natriuretic peptide levels were measured during symptom-limited, graded exercise on a cycle ergometer in seven male orthotopic cardiac transplant recipients. 2. Resting plasma atrial natriuretic peptide was significantly higher in the transplant recipients than in two control groups, one matched to the transplant recipients (group 1) and the other to the age of the donor heart (group II). 3. The response to exercise of the cardiac transplant recipients was compared with the response of control group II. Mean maximal work load achieved with exercise was around 40% lower in the cardiac transplant recipients. During exercise, plasma atrial natriuretic peptide levels increased in both the cardiac transplant recipients and the control subjects. The increase in plasma atrial natriuretic peptide with exercise was greater in absolute, but less in percentage, terms in transplant recipients than in the control subjects. 4. The increase in mean arterial pressure with exercise was similar in patients and in control subjects; however, heart rate increased in the patients by only 33% compared with a rise of 151% in the control group. 5. These results provide insight into the control of the sodium regulatory hormone atrial natriuretic peptide. First, factors other than a change in heart rate appear of importance in the regulation of atrial natriuretic peptide. Secondly, these findings suggest that cardiac innervation is not of dominant importance in the modulation of atrial natriuretic peptide secretion.

Abnormal rhythmic oscillations of atrial natriuretic peptide and brain natriuretic peptide in heart failure

2003 ◽  
Vol 104 (3) ◽  
pp. 303-312 ◽  
Author(s):  
Hans BENTZEN ◽  
Robert S. PEDERSEN ◽  
Henrik B. PEDERSEN ◽  
Ole NYVAD ◽  
Erling B. PEDERSEN
Keyword(s):  
Heart Failure ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Left Ventricular ◽  
Control Group ◽  
Pulsatile Secretion ◽  
Main Frequency ◽  
Healthy Humans ◽  
Atrial Natriuretic

The purpose of this study was to clarify whether the secretions of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are pulsatile in patients with chronic heart failure (CHF), and whether the rhythmic oscillations for ANP and BNP are abnormal in patients with CHF. Several reports have shown that ANP and especially BNP are valuable indicators of the prognosis in CHF. Previously, a pulsatile secretion has been described for ANP and BNP in healthy humans and for ANP in CHF patients. More information about the secretion pattern of BNP in heart failure is necessary to increase the clinical usefulness of BNP in patients with CHF. Patients with left ventricular systolic dysfunction and CHF (n = 12) and controls (n = 12) were investigated. Plasma ANP and BNP levels were determined every 2min during a 2-h period by radioimmunoassay and analysed for pulsatile behaviour by Fourier transformation. All patients and controls had significant rhythmic oscillations in plasma ANP levels, and 11 patients with CHF and 10 controls had significant rhythmic oscillations in plasma BNP levels. The amplitude of the main frequency was considerably higher in patients with CHF than in controls (ANP: CHF, 4.76pmol/l; controls, 0.75pmol/l; P<0.01. BNP: CHF, 3.24pmol/l; controls, 0.23pmol/l; P<0.001; all values are medians), but the main frequency did not differ significantly between the group with CHF and the control group for either ANP or BNP. Patients with CHF demonstrate pulsatile secretion of ANP and BNP with a much higher absolute amplitude, but with the same main frequency as healthy subjects.

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