atrial-natriuretic-factor and Pulmonary-Edema

Natriuretic peptides (NPs) are released from the heart in response to pressure and volume overload. B-type natriuretic peptide (BNP) and N-terminal-proBNP have become important diagnostic tools for assessing patients who present acutely with dyspnea. The NP level reflects a compilation of systolic and diastolic function as well as right ventricular and valvular function. Studies suggest that using NPs in the emergency department can reduce the consumption of hospital resources and can lower costs by either eliminating the need for other, more expensive tests or by establishing an alternative diagnosis that does not require hospital stay. Caveats such as body mass index and renal function must be taken into account when analyzing NP levels. Natriuretic peptide levels have important prognostic value in multiple clinical settings, including in patients with stable coronary artery disease and with acute coronary syndromes. In patients with decompensated heart failure due to volume overload, a treatment-induced drop in wedge pressure is often accompanied by a rapid drop in NP levels. Knowing a patient's NP levels might thus assist with hemodynamic assessment and subsequent treatment titration. Monitoring NP levels in the outpatient setting might also improve patient care and outcomes.

Topics: Atrial Natriuretic Factor; Cardiovascular Diseases; Death, Sudden, Cardiac; Heart Diseases; Heart Failure; Hemodynamics; Humans; Kidney Failure, Chronic; Monitoring, Physiologic; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Obesity; Peptide Fragments; Prognosis; Pulmonary Edema; Pulmonary Embolism; Pulmonary Wedge Pressure; Renal Dialysis; Stroke; Weight Loss

High-altitude pulmonary edema is a serious clinical condition observed in individuals participating in mountain climbing and skiing at high altitudes. High-altitude pulmonary edema is an oncardiogenic form of pulmonary edema. Atrial natriuretic factor and endothelin are implicated and ventilatory support is important in preventing fatalities.

Topics: Altitude Sickness; Atrial Natriuretic Factor; Critical Care; Endothelins; Humans; Pulmonary Circulation; Pulmonary Edema

Topics: Animals; Atrial Natriuretic Factor; Guanylate Cyclase; Heart Failure; Humans; Lung; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Nerve Tissue Proteins; Pulmonary Edema; Receptors, Atrial Natriuretic Factor

OBJECTIVE AND DATA SOURCE: Experimental and clinical data reported in the international literature have been collected and critically reviewed to summarize knowledge of the role of atrial natriuretic factor (ANF) in lung physiology and pathophysiology.. Lung contribution to circulating ANF concentration is modest, whereas its capability of degrading ANF is very high, the lung being one of the major sites of ANF catabolism. The impairment of ANF protease activity in lung tissue by hypoxia and pulmonary hypertension could be responsible for the increase in ANF plasma levels observed in several pulmonary pathological conditions. ANF-specific binding sites in lung are reportedly greater than in any other tissue. ANF induces a cGMP-mediated relaxation of central (rather than peripheral) bronchi. ANF bronchodilating effect has also been clinically demonstrated; eg, asthmatic patients show increased plasma ANF levels and exogenous ANF infusion provokes bronchial relaxation comparable with the salbutamol-induced effect. Moreover, ANF determines pulmonary artery vasodilation, thus contributing to improved pulmonary circulation. When pathophysiological levels are present in plasma, ANF influences pulmonary fluid regulation provoking protein mobilization from arteries to the alveolar space whereas ANF pharmacological concentrations re-equilibrate the transwall gradient. A remarkable enhancement of guanylate cyclase activity in lung tissue before hemodynamic modifications by both endogenous end exogenous ANF has been reported in pneumocytes of cardiomyopathic hamsters. On the other hand, ANF infusion provokes a reduction of pulmonary edema induced by pneumotoxic chemicals through a mechanism independent of the natriuretic/hypotensive action of the peptide and not mediated by cGMP.. The modest amount of specific research on ANF effects on lung does not permit a final assessment of natriuretic peptides in pulmonary physiology and pathophysiology. In particular, further investigations are needed to determine the potential clinical relevance of ANF in asthma and pulmonary edema.

Topics: Animals; Atrial Natriuretic Factor; Cyclic GMP; Humans; Lung; Lung Diseases; Pulmonary Edema

Topics: Atrial Natriuretic Factor; Humans; Pericarditis, Constrictive; Pulmonary Edema

Atrial natriuretic peptide (ANP) has a variety of pharmacologic effects, including natriuresis, diuresis, vasodilatation, and suppression of the reninangiotensin system. A recent study showed that ANP infusion improved hypoxemia and pulmonary hypertension in a lung injury model. On the other hand, the pulse contour cardiac output (PiCCO(TM)) system (Pulsion Medical Systems, Munich, Germany) allows monitoring of the intravascular volume status and may be used to guide volume therapy in severe sepsis and critically ill patients.. We treated 10 pulmonary edema patients without heart disease with human ANP (HANP). The patients were divided into two groups: a group with normal Intrathoracic Blood Volume (ITBV) (900-1100 mL/m(2)) (n = 6), and a group with abnormal ITBV (n = 4), as measured by the PiCCO(TM) device; the extravascular lung water (EVLW) and pulmonary vascular permeability index (PVPI) in the two groups were compared.. The average patient age was 63.9 +/- 14.4 years. The normal ITBV group showed significant improvement of the EVLW (before, 16.7 +/- 2.7 mL/kg; after, 10.5 +/- 3.6 mL/kg; p = 0.0020) and PVPI (before, 3.2 +/- 0.3; after, 2.1 +/- 0.7; p = 0.0214) after the treatment. The abnormal ITBV group showed no significant improvement of either the EVLW (before, 16.3 +/- 8.9 mL/kg; after, 18.8 +/- 9.6 mL/kg; p = 0.8387) or PVPI (before, 2.3 +/- 0.8; after, 2.7 +/- 1.3; p = 0.2782) after the treatment. In both groups, the EVLW and PVPI were strongly correlated with the chest X-ray findings.. We conclude that HANP supplementation may improve the EVLW and PVPI in pulmonary edema patients without heart disease with a normal ITBV. The PiCCO(TM) system seems to be a useful device for the management of pulmonary edema.

Topics: Aged; Atrial Natriuretic Factor; Cardiac Output; Female; Humans; Injections, Intravenous; Male; Middle Aged; Monitoring, Physiologic; Pulmonary Edema

We evaluated the effects of human natriuretic peptide (hANP) on the recipients of living-related renal transplantation in children. Anesthesia was maintained with nitrous-oxide and isoflurane in oxygen. The recipients were divided into two groups: the hANP group (n = 8) received continuous infusion of hANP (0.1 microgram.kg-1.min-1), and the control group (n = 5) received no hANP infusion. Intravenous hANP infusion was started at the loading time of fresh frozen plasma in the recipients until the 12 hours after operation. There were no differences between the groups with regards to age, height, body weight, changes in heart rate and systolic arterial pressure, urine volume during operation, and the levels of blood uremic nitrogen and creatinine. The hANP group showed minimal change in CVP during operation and body weight between the values during and after operation compared with control group. The control group needed significantly more fluid than hANP group during operation. We concluded that continuous i.v. hANP infusion in the pediatric recipients of living-related renal transplantation was useful for maintaining sufficient urination and prevention of heart failure or lung edema.

Topics: Anesthesia, General; Atrial Natriuretic Factor; Child; Child, Preschool; Heart Failure; Humans; Infusions, Intravenous; Intraoperative Complications; Kidney Transplantation; Living Donors; Perioperative Care; Pulmonary Edema; Urination

Atrial Natriuretic Peptide (ANP) is secreted in response to hypoxia and pulmonary vasoconstriction. The hormone modulates pulmonary vascular tone in vivo and decreases pulmonary edema in isolated lungs exposed to several toxic agents. In addition, ANP improves the barrier function of endothelial cell monolayers in vitro. The plasma levels of ANP are elevated in patients with high-altitude pulmonary edema. We hypothesized that under these circumstances, ANP improves pulmonary gas exchange by attenuating the transvascular permeation of plasma (water). Therefore, we studied the effect of low-dose ANP in 11 healthy mountaineers exposed to hypoxia in a single-blind, placebo-controlled, cross-over design. During four 1-h periods, the subjects were stepwise exposed to decreasing barometric pressure, with a minimum of 456 mm Hg (simulated altitude, 4,115 m). Infusion of 5 ng/kg/min human-ANP increased the plasma ANP concentrations approximately twofold. The plasma concentrations of cyclic GMP, which is the second messenger of ANP, rose approximately threefold. Infusion of ANP did not affect the hemodynamic or ventilatory response to hypoxia. The hemoglobin concentration, however, rose from 9.0 +/- 0.1 to 9.4 +/- 0.1 mmol/L (p < 0.01) during ANP infusion but not during placebo infusion. The change in plasma volume calculated from this hemoconcentration indicated that approximately 10% of the plasma volume had permeated into the interstitium. Despite the observed whole-body hemoconcentration, oxygen saturation was significantly higher during ANP infusion than during placebo infusion (84.7 +/- 1.7 versus 79.6 +/- 1.8%, p < 0.05), and the alveolar-arterial oxygen difference was significantly lower (3.5 +/- 0.7 versus 7.3 +/- 0.8 mm Hg, p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Blood Proteins; Carbon Dioxide; Cyclic GMP; Heart Rate; Hemoglobins; Humans; Hypoxia; Infusions, Intravenous; Mountaineering; Oxygen; Oxygen Consumption; Partial Pressure; Placebos; Plasma Volume; Pulmonary Edema; Pulmonary Gas Exchange; Single-Blind Method

Carperitide is used to treat acute heart failure (AHF) in Japan. Whether the degree of pulmonary congestion is associated with the effects of carperitide on AHF is unclear.Methods and Results:We retrospectively investigated the in-hospital outcomes and prognoses of 742 patients hospitalized for AHF between February 2015 and January 2017 and classified them into carperitide and non-carperitide groups, stratified according to the degree of pulmonary congestion. The median follow-up duration after admission was 231 days. In patients with moderate-severe pulmonary congestion, the rate of remaining congestion on chest X-ray at discharge was lower in the carperitide group than in the non-carperitide group (1.5% vs. 9.0%, P=0.004). Also, the carperitide group had significant reduction in a composite of all-cause death or rehospitalization for HF (adjusted hazard ratio, 0.62; 95% CI: 0.41-0.93; P=0.02). In patients with no-mild pulmonary congestion, carperitide was not associated with better clinical outcome.. In the treatment of AHF with moderate-severe pulmonary congestion, carperitide is associated with more effective decongestion in the short term and better prognosis in the long term.

Topics: Acute Disease; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Cause of Death; Heart Failure; Hospitalization; Humans; Male; Prognosis; Pulmonary Edema; Retrospective Studies

Atrial natriuretic peptide (ANP) inhibits agonist-induced pulmonary edema formation, but the signaling pathway responsible is not well defined. To investigate the role of the particulate guanylate cyclase-linked receptor, natriuretic peptide receptor-A (NPR-A), we measured acute lung injury responses in intact mice and pulmonary microvascular endothelial cells (PMVEC) with normal and disrupted expression of NPR-A. NPR-A wild-type (NPR-A+/+), heterozygous (NPR-A+/-), and knockout (NPR-A-/-) mice were anesthetized and treated with thrombin receptor agonist peptide (TRAP) or lipopolysaccharide (LPS). Lung injury was assessed by lung wet-to-dry (W/D) weight and by protein and cell concentration of bronchoalveolar lavage (BAL) fluid. No difference in pulmonary edema formation was seen between NPR-A genotypes under baseline conditions. TRAP and LPS increased lung W/D weight and BAL fluid cell counts more in NPR-A-/- mice than in NPR-A+/- or NPR-A+/+ mice, but no genotype-related differences were seen in TRAP-induced increases in bloodless lung W/D weight or LPS-induced increases in BAL protein concentration. Pretreatment with ANP infusion completely blocked TRAP-induced increases in lung W/D weight and blunted LPS-induced increases in BAL cell counts and protein concentration in both NPR-A-/- and NPR-A+/+ mice. Thrombin decreased transmembrane electrical resistance in monolayers of PMVECs in vitro, and this effect was attenuated by ANP in PMVECs isolated from both genotypes. Administration of the NPR-C-specific ligand, cANF, also blocked TRAP-induced increases in lung W/D weight and LPS-induced increases in BAL cell count and protein concentration in NPR-A+/+ and NPR-A-/- mice. We conclude that ANP is capable of attenuating agonist-induced lung edema in the absence of NPR-A. The protective effect of ANP on agonist-induced lung injury and pulmonary barrier function may be mediated by NPR-C.

Topics: Animals; Atrial Natriuretic Factor; Bronchoalveolar Lavage Fluid; Capillary Permeability; Cells, Cultured; Endothelial Cells; Endothelium, Vascular; Lipopolysaccharides; Lung Injury; Mice; Natriuretic Peptide, C-Type; Pulmonary Edema; Receptors, Atrial Natriuretic Factor; Receptors, Guanylate Cyclase-Coupled; Receptors, Peptide; Receptors, Thrombin; Signal Transduction; Thrombin

Recently, an increase in extravascular lung water (EVLW) accumulation with diminished left ventricular contractility within 60 min after SCUBA diving was reported. We have observed previously that diving was associated with reduced diffusing lung capacity for carbon monoxide (DLCO) and arterial oxygen pressure for up to 60-80 min postdive. Here we investigated whether increased EVLW persists 2-3h after successive deep dives in a group of seven male divers. The echocardiographic indices of pulmonary water accumulation (ultrasound lung comets (ULC)) and left ventricular function, respiratory functional measurements and arterial oxygen saturation (SaO(2)) were assessed 2-3h post diving, while venous gas bubbles (VGB) and the blood levels of NT-proBNP and proANP were analyzed 40 min after surfacing. Spirometry values, flow-volume, DLCO, SaO(2) and ULC were unchanged after each dive, except for significant increase in ULC after the second dive. Left ventricular function was reduced, while NT-proBNP and proANP levels were significantly elevated after majority of dives, suggesting a cardiac strain.

Topics: Adult; Atrial Natriuretic Factor; Decompression Sickness; Diving; Extravascular Lung Water; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Oxygen; Peptide Fragments; Pulmonary Diffusing Capacity; Pulmonary Edema; Spirometry; Time Factors; Ultrasonography; Ventricular Function, Left

Daily changes in serum concentrations of natriuretic peptides and various cardiopulmonary parameters were measured after the onset of subarachnoid hemorrhage (SAH) to investigate the pathogenesis of the cardiac and pulmonary consequences in 15 patients with acute phase SAH, divided into the control group (n = 5) with consciousness continuously preserved from SAH onset to admission, and the consciousness disturbance group (n = 10). Daily changes in serum A-type and B-type natriuretic peptides (ANP and BNP, respectively) were measured for 10 days, and intrathoracic blood volume index and extravascular lung water index (EVLWI) were measured for 5 days by the single transpulmonary thermodilution method. Natriuretic peptides in the consciousness disturbance group showed significantly higher values during the 10-day period, with ANP 119.2 +/- 12.4 pg/ml (mean +/- standard error of the mean, p = 0.005) on day 2 and BNP 354.1 +/- 80.3 pg/ml (p = 0.009) on day 1. EVLWI showed higher values in the consciousness disturbance group compared to the control group throughout the 5-day period. The increases in natriuretic peptide levels and increase in pulmonary extravascular water content found in SAH patients with consciousness disturbance show that load on the left ventricle or atrium as well as pulmonary capillary pressure are increased immediately after onset, supporting the contention that excessive release of catecholamines occurs at this time.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Blood Volume; Catecholamines; Extravascular Lung Water; Female; Humans; Hyponatremia; Male; Middle Aged; Natriuretic Peptide, Brain; Pulmonary Edema; Sodium; Subarachnoid Hemorrhage; Thermodilution; Unconsciousness

Atrial natriuretic peptide is regarded as an important regulator of pulmonary vasomotor tone and permeability. This study investigated the role of atrial natriuretic peptide in sepsis-associated pulmonary pathophysiology.. Prospective experimental investigation.. Laboratory at a university hospital.. Twelve awake, chronically instrumented sheep.. The sheep were instrumented with lung lymph fistulas and received a continuous infusion with live Pseudomonas aeruginosa for 48 hrs. After 40 hrs, the atrial natriuretic peptide-receptor antagonist HS-142-1 was continuously infused in the HS-124-1 group (3 mg/kg/hr, n = 6) for 8 hrs, whereas the control group received the carrier (n = 6).. Lung lymph flow was markedly elevated in response to sepsis after 40 hrs in both groups. Atrial natriuretic peptide-receptor blockade further increased lymph flows by 41 +/- 17% (41 hrs) up to 64 +/- 20% (44 hrs, p < .05) in the presence of normal permeability to protein. Although mean pulmonary artery pressure increased (p < .05 vs. 40 hrs), capillary pressure remained unaffected. Despite identical fluid balances in both groups, cardiovascular filling variables significantly increased in the HS-142-1 group. This was associated with increasing cardiac index and mean arterial pressure (p < .05 vs. 40 hrs). In the control group, all variables remained constant between 41 and 48 hrs.. Blockade of atrial natriuretic peptide receptors increases pulmonary transvascular fluid flux independent of changes in permeability to protein in chronic ovine sepsis. Atrial natriuretic peptide may therefore play a protective role for the alveolar-capillary barrier during sepsis.

Topics: Animals; Atrial Natriuretic Factor; Disease Models, Animal; Female; Lung; Lymphatic System; Male; Permeability; Pseudomonas Infections; Pulmonary Circulation; Pulmonary Edema; Receptors, Atrial Natriuretic Factor; Reference Values; Risk Factors; Sensitivity and Specificity; Sepsis; Sheep, Domestic

The purpose of this study was to examine and compare the effects of atrial natriuretic peptide and furosemide on pulmonary gas exchange, hemodynamics, extravascular lung water, and renal function in a dog model of oleic acid-induced pulmonary edema.. Prospective, comparable, experimental study.. Laboratory at a university hospital.. Eighteen male beagle dogs were studied under mechanical ventilation with pentobarbital anesthesia.. Oleic acid (0.08 mL/kg) was injected and allowed for 1 hr to achieve pulmonary edema with hypoxemia at Fio2 of 0.3. After lung injury, dogs were divided into three groups; control group (n = 6) receiving saline (2.5 mL/hr for 5 hrs), atrial natriuretic peptide group (n = 6) receiving atrial natriuretic peptide (1 microg x kg(-1) x min(-1) for 5 hrs), and furosemide group (n = 6) receiving furosemide (1 mg x kg(-1) x hr(-1) for 5 hrs).. Hemodynamics, arterial blood gases, extravascular lung water, and renal function were measured hourly for 7 hrs after injury. Oleic acid increased extravascular lung water and induced hypoxemia. In the atrial natriuretic peptide group, extravascular lung water was significantly (p <.05) lower and Pao2 was significantly (p <.05) higher than in the control and furosemide groups, respectively. Pulmonary hypertension induced by oleic acid was attenuated by atrial natriuretic peptide infusion but not by saline or furosemide. Increased natriuresis/diuresis did not significantly differ between the atrial natriuretic peptide and the furosemide group, whereas creatinine clearance in the atrial natriuretic peptide group was significantly higher than that in the furosemide group.. These findings suggest that atrial natriuretic peptide improves pulmonary gas exchange by reducing extravascular lung water and pulmonary arterial pressure, possibly independently from natriuresis/diuresis in oleic acid-induced pulmonary edema.

Topics: Animals; Atrial Natriuretic Factor; Diuretics; Dogs; Extravascular Lung Water; Furosemide; Hemodynamics; Kidney; Male; Oleic Acid; Pulmonary Edema; Pulmonary Gas Exchange

High altitude pulmonary edema (HAPE) is associated with increases in pulmonary arterial and hydrostatic pressures and an increase in pulmonary vascular permeability. There is evidence to suggest that inflammatory mediators may cause some forms of HAPE, and Salmonella enteritidis endotoxin (ETX) is known to activate neutrophils and inflammatory mediators, such as TNF-alpha and IL1-beta. Since HAPE has been produced in rats primed with ETX, we hypothesized that ANP release and action may ameliorate HAPE and that ANP blockade may exacerbate HAPE in ETX-primed rats exposed to high altitude (HA). Plasma ANP, right atrial ANP mRNA, and indexes of lung injury were measured in rats primed with endotoxin (ETX) (0.1 mg/kg BW, i.p.) and exposed to simulated HA (4267 m; P(B) = 440 mmHg) for either 12 or 24 h. Catheters were chronically inserted into the right carotid artery, pulmonary artery, and jugular vein for assessment of hemodynamic parameters in response to ETX and/or HA. In addition, some rats were injected with an antibody against ANP (alphaANP) prior to normoxic (NX) or HA exposure. Pulmonary arterial pressure increased in the alphaANP group (50 +/- 20%; p < or = 0.05) and in the HA + alphaANP (51 +/- 15%; p < or = 0.05) group at 12 h compared to NX sham rats injected with normal rabbit serum. In addition, systemic arterial pressure was significantly lower in the HA + ETX rats compared to HA + ETX + alphaANP rats (p < or = 0.001). Plasma ANP levels were significantly higher at 12 and 24 h in ETX, HA, and HA + ETX groups (p

Topics: Altitude Sickness; Animals; Antibodies; Atrial Natriuretic Factor; Blood Pressure; Endotoxins; Male; Pulmonary Edema; Rats; Rats, Sprague-Dawley; Salmonella enteritidis

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 pg x ml(-1), P<0.01; 33.1 versus 6.8 ng x g(-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.

Topics: Animals; Atrial Natriuretic Factor; Cyclic GMP; Lung; Male; Pneumonectomy; Postoperative Complications; Pulmonary Edema; Rats; Rats, Wistar; Receptors, Atrial Natriuretic Factor; RNA, Messenger

The effect of moderate left atrial (LA) hypertension on alveolar liquid clearance (ALC) was investigated in anesthetized, ventilated sheep, surgically prepared to measure lung lymph flow as well as hemodynamics. To simulate alveolar edema, 3-4 ml/kg of isosmolar 5% albumin in Ringer lactate were instilled into each lower lobe, and ALC was measured. After 4 h of LA hypertension (24 cmH2O), ALC was similar to that in control sheep (31 +/- 3% with LA hypertension vs. 34 +/- 10% with normal LA pressure). Because plasma epinephrine levels were moderately elevated in the presence of LA hypertension, ALC was then studied in the presence of LA hypertension following bilateral adrenalectomy. Without endogenous release of epinephrine, ALC was significantly reduced compared with normal LA pressure (20 +/- 7% compared with 34 +/- 10%, P < 0.05). Thus endogenous catecholamines caused a submaximal stimulation of ALC in the presence of LA hypertension. Exogenous administration of aerosolized beta2-agonist therapy with salmeterol increased ALC in the presence of normal LA pressure but had no stimulatory effect in the presence of moderate LA hypertension. Therefore, we tested the hypothesis that endogenous release of atrial natriuretic factor (ANF) may downregulate alveolar epithelial Na+ and fluid transport in the presence of LA hypertension. There was a modest twofold increase in plasma ANF levels after LA hypertension. Additional in vitro studies demonstrated that, in the presence of beta2-agonist stimulation, ANF decreased Na+ pump activity (Na+-K+-ATPase) in isolated rat alveolar epithelial type II cells. ANF may downregulate vectorial Na+ and fluid transport stimulated by endogenous or exogenous beta-adrenergic agonist stimulation in the presence of LA hypertension. In summary, ALC continues even in the presence of moderate LA hypertension. Aerosolized beta2-adrenergic agonist therapy significantly increased ALC, but only when LA pressure was normal.

Topics: Adrenalectomy; Adrenergic alpha-Agonists; Anesthesia; Animals; Atrial Natriuretic Factor; Blood Proteins; Capillary Permeability; Epinephrine; Hemodynamics; Hypertension; In Vitro Techniques; Lymph; Male; Pulmonary Alveoli; Pulmonary Edema; Rats; Rats, Sprague-Dawley; Respiration, Artificial; Sheep; Sodium-Potassium-Exchanging ATPase

A 19-year-old female was scheduled for living-related kidney transplantation under general anesthesia. Eight units of fresh frozen plasma were infused in 30 minutes before the recanalization of renal vessels. Twenty minutes after the first urination, end-tidal-CO2 suddenly increased showing CVP of 18 mmHg. We considered that she had developed acute pulmonary edema. Continuous hANP infusion was initiated at the rate of 0.1 microgram.kg-1.min-1. By this infusion, end-tidal-CO2 and CVP gradually decreased and operation was concluded successfully. This case demonstrates that hANP works also on the transplanted kidney.

Topics: Acute Disease; Adult; Anesthesia, General; Atrial Natriuretic Factor; Female; Humans; Infusions, Intravenous; Intraoperative Care; Intraoperative Complications; Kidney Transplantation; Living Donors; Pulmonary Edema

Because atrial natriuretic peptide (ANP) is considered to play a role in lung physiology and pathology, our aim was to characterize natriuretic peptide receptors in cultured rat alveolar type II (ATII) cells. Guanylate cyclase A- and B-receptor but not clearance-receptor mRNAs were detected by reverse transcription-polymerase chain reaction. The absence of clearance-receptor expression in ATII cells was confirmed by competitive inhibition of ANP binding; ANP (0.1-100 nM) decreased the binding of 125I-ANP, whereas C-ANP-(4-23), a specific ligand of clearance receptors, was ineffective. ANP induced a dose-dependent increase in guanosine 3',5'-cyclic monophosphate (cGMP) production, with a threshold of 0.1 nM, whereas the response to C-type natriuretic peptide was weak and was observed only at high concentrations (100 nM). In ATII cells cultured on filters, 1) ANP receptors were present on both the apical and basolateral surfaces and 2) cGMP egression was polarized, as indicated by the greater ANP-induced cGMP accumulation in the basolateral medium, and was partially inhibited by probenecid, an organic acid transport inhibitor. Influx studies demonstrated that ANP decreased the amiloride-sensitive component of 22Na influx but did not change ouabain-sensitive 86Rb influx. In conclusion, ATII cells behave as a target for ANP. ANP activation of guanylate cyclase A receptors produces cGMP, which is preferentially extruded on the basolateral side of the cells and inhibits the amiloride-sensitive Na-channel activity.

Topics: Amiloride; Animals; Atrial Natriuretic Factor; Cells, Cultured; Cyclic GMP; Diuretics; Guanylate Cyclase; Peptide Fragments; Polymerase Chain Reaction; Pulmonary Alveoli; Pulmonary Edema; Rats; Receptors, Atrial Natriuretic Factor; RNA, Messenger; Rubidium; Sodium

To test the effect of atrial natriuretic peptide (ANF) in dogs with acute pulmonary edema in the absence of urinary sodium retention. ANF is normally a potent natriuretic agent, although this effect is attenuated in generalized edema or acute renal failure.. Animal study.. Twenty-nine dogs.. Induction of acute pulmonary edema with intravenously administered alloxan and administration of ANF according to five protocols.. Natriuretic effect of ANF before and after the induction of pulmonary edema during the protocols.. In six control animals, induction of pulmonary edema was associated with diuresis (mean 0.38, standard error of the mean [SEM] 0.003 mL/min before alloxan administration v. mean 0.75, SEM 0.11 mL/min after); natriuresis (mean 60, SEM 8 mumol/min before v. mean 103, SEM 12 mumol/min after); and a decline in blood pressure (mean 114, SEM 7 mm Hg before v. mean 93, SEM 9 mm Hg after) and in the glomerular filtration rate (mean 52, SEM 3.3 mL/min before v. mean 36, SEM 3.7 mL/min after). When isoncotic dextran solution was infused in dogs with pulmonary edema, blood pressure was maintained but the glomerular filtration rate still declined by 42% and there was natriuresis. When the renal arteries were clamped for 5 minutes during the infusion of alloxan, diuresis and natriuresis were prevented, but the glomerular filtration rate still declined, although blood pressure was maintained. ANF administered intravenously during pulmonary edema induced a further significant natriuresis in all experimental protocols. Catalase, administered intravenously as a bolus just before the alloxan infusion, prevented pulmonary edema and the associated renal changes.. Although alloxan appears to be directly nephrotoxic, renal damage caused by this compound does not impair the natriuretic effect of ANF in acute pulmonary edema.

Topics: Acute Disease; Alloxan; Animals; Atrial Natriuretic Factor; Catalase; Diuresis; Dogs; Female; Glomerular Filtration Rate; Kidney; Male; Natriuresis; Pulmonary Edema

Ozone can cause pulmonary edema and simultaneously decrease blood pressure. Atrial natriuretic peptides may mediate both of these affects since they increase pulmonary capillary permeability and are potent vasodilating peptides. To examine this possibility and determine if aged animals respond differently to ozone, adult (4-6 months old) and aged (24-26 months old) Fischer 344 rats were exposed to ozone (0.5 parts per million) for 8 h. Ozone increased atrial natriuretic peptides recognized by the proANF 1-30, proANF 31-67, and atrial natriuretic factor (ANF) radioimmunoassays in lung from 3.7 +/- 0.2, 3.5 +/- 0.1, and 3.0 +/- 0.2 ng/g of lung, respectively, to 9.7 +/- 1.0, 9.2 +/- 0.4, and 13.3 +/- 2.7 ng/g in adult rats (n = 6) and from 3.6 +/- 0.1, 3.5 +/- 0.1, and 3.2 +/- 0.1 ng/g of lung of aged rats (n = 6) to 10.2 +/- 0.3, 10.0 +/- 0.2, and 12.6 +/- 0.2 ng/g. Ozone increased the content of these peptides in the heart 2- to 5-fold from 266 +/- 25, 226 +/- 22, and 288 +/- 40 ng/g of heart to 716 +/- 26, 471 +/- 14, and 1,473 +/- 235 ng/g in the same adult animals and from 495 +/- 17, 483 +/- 22, and 501 +/- 18 ng/g to 903 +/- 16,879 +/- 21, and 1,489 +/- 31 ng/g of heart in the aged animals. Ozone also doubled the concentration of these atrial natriuretic peptides in the circulatory system. This study demonstrates that ozone increases atrial natriuretic peptides in the lung, heart, and circulation of equal magnitude in aged versus adult animals, indicating an equal response to ozone with aging. This study further suggests that atrial natriuretic peptides may mediate the decreased blood pressure and pulmonary edema observed with ozone exposure.

Topics: Aging; Animals; Atrial Natriuretic Factor; Blood Pressure; Heart; Lung; Male; Myocardium; Ozone; Peptide Fragments; Protein Precursors; Pulmonary Edema; Rats; Rats, Inbred F344

Previous studies reported that atrial natriuretic factor (ANF) decreased lung edema in guinea pigs. To determine whether ANF protects against lung edema by increasing active Na+ transport and lung edema clearance, ANF (10(-7) M) was instilled into the air spaces (n = 5) or perfused through the pulmonary circulation (n = 5) of isolated perfused liquid-filled rat lungs. These animals were compared with five control rats and four rats having amiloride (10(-5) M) instilled into the air space. Amiloride reduced lung edema clearance by 65%, perfused ANF reduced lung edema clearance by 32%, and instilled ANF did not change edema clearance compared with responses in control rats after 70 min of experimental protocol. Passive Na+ movement increased by 91% with perfused ANF and by 52% with instilled ANF compared with that in control rats. Albumin flux from the perfusate into the air space increased in ANF-perfused lungs compared with control lungs (P < 0.05) but not when ANF or amiloride was instilled into the air spaces. These results suggest that ANF instilled into rat air spaces or perfused through the pulmonary circulation increases lung epithelial permeability and that ANF perfused through the pulmonary circulation decreases lung edema clearance due to impaired active Na+ transport. Conceivably, the previously observed protective effect of ANF was due to reduced pressures across the pulmonary circulation, which resulted in less edema formation.

Topics: Amiloride; Animals; Atrial Natriuretic Factor; Biological Transport, Active; Blood Pressure; Capillary Permeability; Cyclic GMP; Epithelium; Male; Perfusion; Pulmonary Alveoli; Pulmonary Edema; Rats; Rats, Sprague-Dawley; RNA; Sodium; Time Factors

This study was designed to address three objectives in an experimental model of acute congestive heart failure (CHF) in the dog produced by rapid ventricular pacing. The first objective was to characterize cardiorenal and humoral responses before and during 2 h of acute CHF. The second objective was to determine the modulating action of iv furosemide upon these biologic responses to acute CHF, testing the hypothesis that furosemide-mediated natriuresis is associated with activation of the renin-angiotensin-aldosterone system (RAAS) compared with the control group. The third objective was to determine the modulating action of continuous low-dose atrial natriuretic factor (ANF) administration during acute CHF upon these biologic responses, testing the hypothesis that exogenous low-dose ANF would prevent activation of the RAAS and enhance the natriuretic action of furosemide. In the control group (Group 1; N = 6), plasma ANF increased after the onset of CHF; GFR and sodium excretion were maintained without activation of this RAAS despite arterial hypotension. In Group 2 (N = 6), furosemide in acute CHF increased sodium excretion but in association with a decrease in GFR and activation of the RAAS. Low-dose exogenous ANF and furosemide (Group 3; N = 6) in acute CHF were associated with a maintenance of GFR, no activation of the RAAS, and potentiation of furosemide-induced natriuresis. In summary, these studies demonstrate that furosemide potently increases sodium excretion in acute CHF, but with a decrease in GFR and activation of the RAAS. Low-dose ANF in acute CHF with furosemide maintains GFR, attenuates activation of the RAAS, and potentiates natriuresis.

Topics: Acute Disease; Angiotensin II; Animals; Atrial Natriuretic Factor; Dogs; Drug Synergism; Drug Therapy, Combination; Female; Furosemide; Heart Failure; Male; Natriuresis; Pulmonary Edema; Renin-Angiotensin System

The postdialytic plasma level of cGMP, a marker for the release of atrial natriuretic peptide (ANP) in humans, is closely related to hypervolemia in chronic hemodialysis patients. In order to test the practicability of routine postdialysis cGMP determination for the detection of fluid overload, ANP and cGMP levels in the total hemodialysis population of 81 patients were measured with blood samples drawn immediately after hemodialysis. Twenty-three patients had a cGMP level of more than 20 pmol/mL. In 13 of these, pulmonary congestion was present on the chest roentgenogram. Two of these patients refused a gradual reduction of their dry body weight. In the remaining 21 patients, the weight reduction was associated with a decrease in cGMP levels in all cases and with a decrease in ANP levels in all but two cases. Fourteen of the 21 patients reached a cGMP level below 20 pmol/mL after weight reduction, and at that time, none of these showed signs of pulmonary congestion on chest x-ray. All seven patients, whose cGMP levels remained above 20 pmol/mL despite the reduction, had documented heart disease with impairment of left ventricular function. These results suggest that the plasma cGMP level after hemodialysis is more apt for the determination of dry body weight than is ANP or a chest roentgenogram.

Topics: Adult; Aged; Antihypertensive Agents; Atrial Natriuretic Factor; Biomarkers; Body Weight; Cardiovascular Diseases; Cyclic GMP; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Nitric Oxide; Predictive Value of Tests; Pulmonary Edema; Radiography; Renal Dialysis; Ventricular Function, Left; Water-Electrolyte Imbalance

We investigated the effects of acute hypoxia (10% O2) on plasma level of atrial natriuretic peptide (ANP) and pulmonary hemodynamics in five subjects with a history of high-altitude pulmonary edema (HAPE). Plasma renin activity and plasma levels of aldosterone, epinephrine and norepinephrine were also measured. The plasma ANP levels in HAPE-susceptible subjects rose significantly in response to 10% O2 (from 34.8 +/- 5.4 to 51.4 +/- 7.3 pg.ml-1; P less than 0.05), not associated with any increase in either atrial pressure. Compared with six control subjects, the rise of ANP level was greater in HAPE-susceptible subjects (16.6 +/- 4.4 vs 3.9 +/- 1.2 pg.ml-1; P less than 0.05). There was a significant positive correlation between the rise of ANP level and the increase of pulmonary arterial pressure. No significant difference was observed in any of other hormonal responses to acute hypoxia between the two groups. We interpret these results as indicating that the ANP secretory response to acute hypoxia in HAPE-susceptible subjects, which is not mediated by an increase in atrial pressure, may be greater than that in nonsusceptible subjects in association with a greater pressor response of pulmonary circulation.

Topics: Adult; Aldosterone; Altitude; Atrial Natriuretic Factor; Epinephrine; Humans; Hypoxia; Male; Norepinephrine; Pulmonary Circulation; Pulmonary Edema; Renin

Topics: Atrial Natriuretic Factor; Cardiac Tamponade; Heart; Heart Failure; Humans; Pericarditis, Constrictive; Pulmonary Edema

Chemically and enzymatically generated oxidants alter endothelial cell shape, increase macromolecular permeability across endothelial cell monolayers, and increase lung microvascular permeability. We examined the effect of ANP (atrial natriuretic peptide) on oxidant-induced injuries to bovine aortic endothelial cell monolayers and to isolated, perfused rabbit lungs. Treatment of cultured endothelial monolayers with glucose oxidase (1.4 U/ml) caused changes in cell shape characterized by a retraction of cells and the formation of numerous intercellular gaps. Glucose oxidase treatment also caused a reduction in F-actin stress fibers visualized by rhodamine-phalloidin fluorescence. Pretreatment (5 min) of the endothelial monolayers with ANP (10(-7) M) attenuated the oxidant-induced changes in cell shape and reduction in F-actin staining. In addition, ANP significantly (P less than 0.05) reduced increases in endothelial monolayer permeability to albumin resulting from glucose oxidase treatment. Oxidant-induced injury of isolated, perfused rabbit lungs produced pulmonary edema measured as an increase in lung weight. This increase in weight was significantly (P less than 0.05) inhibited by pretreatment of lungs with ANP (10(-7) M). Collectively, these results suggest that ANP may act to preserve endothelial barrier function and reduce edema formation caused by oxidant injury.

Topics: Animals; Atrial Natriuretic Factor; Cattle; Cell Membrane Permeability; Cells, Cultured; Cytoskeleton; Endothelium, Vascular; Oxidants; Pulmonary Edema; Rabbits; Staining and Labeling

Since acute mountain sickness (AMS) is associated with rapid ascent and with fluid retention, we assessed clinical status and fluid homeostasis in men slowly ascending on foot over 3 d to 4559 m and remaining at this altitude 5 d. We studied 15 male mountaineers, 6 of whom had previously had repeated, severe AMS or high altitude pulmonary edema (HAPE), at 1170 m, 3611 m, and 4559 m. We found that four of the six subjects with previous AMS or HAPE compared with none of nine with no such history, developed these conditions. Those who remained well had a diuresis that could not be overcome by increasing fluid intake and no change in renin activity, plasma aldosterone, or atrial natriuretic peptide (ANP). Those who became ill showed considerable weight gain independent of fluid intake, and a great increase in ANP which correlated with measurements of right atrial cross section. We conclude that mountaineers who have previously experienced repeated AMS or HAPE get fluid retention despite slow ascent and that this is associated with widening of the atrium and an increase in ANP.

Topics: Adult; Altitude Sickness; Atrial Natriuretic Factor; Body Fluids; Body Weight; Diuresis; Echocardiography; Heart Atria; Homeostasis; Humans; Male; Middle Aged; Pulmonary Edema; Radiography; Urinary Retention; Water-Electrolyte Balance

The effect of pulmonary injury induced by aspiration of HCl on plasma atrial natriuretic polypeptide (ANP) level was examined in rats given a constant infusion of water and electrolytes. In addition, using specific antiserum against ANP, we investigated the physiological role of ANP in rats after HCl aspiration. Rats were housed individually in metabolic cages and were given a constant infusion of sodium solution via catheters chronically inserted into the jugular vein. Plasma ANP levels were elevated at 3 and 24 h after tracheal injection of 0.2 ml of 0.1 N HCl via the cricothyroid membrane. Urine volume and urinary sodium excretion increased during the first 24 h after acid aspiration. However, this increase was reduced by the injection of anti-ANP serum. Furthermore, the injection of anti-ANP serum resulted in a significant (P less than 0.05) increase in wet lung weight from a value of 0.74 +/- 0.06 (HCl aspiration with normal rabbit serum injection) to 0.83 +/- 0.07% of body weight. These results indicate that ANP plays a physiological role in the regulation of urinary water and sodium excretion after pulmonary acid injury and suggest that ANP elevated in plasma after pulmonary injury may prevent pulmonary edema with its diuretic action and/or some direct action on water movement in the lung.

Topics: Animals; Atrial Natriuretic Factor; Diuresis; Hydrochloric Acid; Lung; Male; Natriuresis; Organ Size; Pulmonary Edema; Rats; Rats, Inbred Strains

Topics: Atrial Natriuretic Factor; Humans; Pulmonary Edema

To verify the presence of the constitutional abnormality implicated in the pathogenesis of high-altitude pulmonary edema (HAPE), we evaluated the hemodynamic responses to hypoxia, hypobaria, and exercise in HAPE-susceptible subjects (HAPE-S). HAPE-S were five males with a history of HAPE. Five healthy volunteers who had repeated experiences of mountain climbing without any history of altitude-related problems served as controls. HAPE-S showed much greater increase in pulmonary vascular resistance index (PVRI) than the control subjects, resulting in a much higher level of pulmonary arterial pressure (Ppa), under both acute hypoxia of 15% O2 (Ppa = 29.0 +/- 2.8 vs. 17.8 +/- 0.3 Torr, P less than 0.05) and acute hypobaria of 515 Torr (32.3 +/- 2.8 vs. 19.1 +/- 0.8 Torr, P less than 0.05). Also, PVRI in HAPE-S exhibited a tendency to increase even during light exercise with supine bicycle ergometer (50 W), whereas PVRI in the control subjects significantly decreased, so that HAPE-S showed a greater increase in Ppa (delta Ppa = 16.0 +/- 1.5 vs. 4.9 +/- 1.1 Torr, P less than 0.001) and a greater decrease in arterial oxygen tension (17.8 +/- 4.7 vs. 5.6 +/- 1.7 Torr, P less than 0.05). We thus conclude that HAPE-S have a constitutional abnormality, which can be evaluated at low altitude, in the pulmonary circulatory responses to possible causative factors of HAPE such as hypoxia, hypobaria, and exercise.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Altitude Sickness; Atmospheric Pressure; Atrial Natriuretic Factor; Blood Gas Analysis; Disease Susceptibility; Hemodynamics; Humans; Hypoxia; Male; Physical Exertion; Pulmonary Edema; Thromboxane B2

It has been established that alpha-hANP, the newly discovered peptide extracted from human cardiac atria, has potent natriuretic and hypotensive actions. Our present investigation is the first to demonstrate that alpha-hANP is capable of protecting against pulmonary edema caused by various chemicals, using isolated perfused guinea pig lung system. Lungs were perfused via pulmonary artery with Krebs-Ringer bicarbonate buffer at 5.0 ml/min, and wet weight of lungs and perfusion pressure of pulmonary artery (Pa) were monitored. Bolus injection of Triton-X or CHAPS into cannulated pulmonary artery produced edema as indicated by a massive increase in wet weight and a slight increase in Pa. Constant infusion of alpha-hANP through pulmonary artery at 200 ng/ml was effective in causing decrease in wet weight of lung. Perfusion of lung with paraquat or PGF2 alpha, and repeated bolus injection of arachidonic acid or PGE2 caused elevation in both wet weight of lung and Pa. The treatment with alpha-hANP similar to that described above also protected against edema caused by paraquat or arachidonic acid. Bolus administration of epinephrine induced a slight increase in wet weight and Pa, and alpha-hANP was effective in decreasing the elevated lung wet weight and Pa of lungs. Infusion or bolus administration of alpha-hANP into control lungs increased cGMP level in outflow perfusate as well as in lung tissue significantly. In lungs with edema which were induced by Triton-X or paraquat, there was a slight increase in cGMP level in Triton-X treated and no increase in paraquat treated lung tissues. In either cases, was there any increase in cGMP level in perfusate. The specific binding study of [125I]alpha-hANP revealed that the lack of increase in cGMP was not due to a loss of receptor in Triton-X or paraquat treated lungs. Thus our study demonstrated that alpha-hANP had a direct anti-edematic action(s) in lung which was not secondary to the systemic natriuretic and/or hypotensive action(s).

Topics: Animals; Arachidonic Acid; Arachidonic Acids; Atrial Natriuretic Factor; Blood Pressure; Cholic Acids; Cyclic GMP; Dinoprost; Dinoprostone; Epinephrine; Guinea Pigs; Humans; Indicator Dilution Techniques; Lung; Male; Norepinephrine; Octoxynol; Organ Size; Paraquat; Peptide Fragments; Polyethylene Glycols; Prostaglandins E; Prostaglandins F; Pulmonary Artery; Pulmonary Edema

A diagnosis of acute high-altitude pulmonary edema was made in five male skiers (age, 35.0 +/- 1.8 years) by history and physical examination and was confirmed by a characteristic chest radiogram showing alveolar infiltrates associated with a normal cardiac silhouette. Five healthy age- and sex-matched subjects with similar physical activity at the same altitude served as controls. Plasma sodium was 135.0 +/- 1.5 mmol/L in the acutely ill patients compared with 144.0 +/- 3.3 mmol/L in the controls (P less than 0.025). Mean plasma atrial natriuretic factor immunoreactivity averaged 17.6 +/- 5.6 pmol/L in patients with high-altitude pulmonary edema compared with 6.8 +/- 0.7 pmol/L in the controls at the same altitude (P less than 0.05). Elevated atrial natriuretic factor levels normalized to 7.5 +/- 1.9 pmol/L (P less than 0.05) during recovery in Denver (altitude, 1600 meters) 24 hours later. Plasma arginine vasopressin levels were 1.8 +/- 0.37 pmol/L in patients with high-altitude pulmonary edema at diagnosis compared with 0.92 +/- 0.28 pmol/L in controls (P = 0.07). The inappropriately elevated arginine vasopressin levels decreased to 1.29 +/- 0.37 pmol/L during recovery (P less than 0.025), but the lowered plasma sodium concentration had not normalized by discharge within 24-hours of transfer to Denver and averaged 135.8 +/- 1.2 mmol/L. The pathophysiologic implications of these findings are discussed.

Topics: Acute Disease; Adult; Aldosterone; Altitude Sickness; Arginine Vasopressin; Atrial Natriuretic Factor; Blood Urea Nitrogen; Creatinine; Humans; Hypoxia; Male; Pulmonary Edema; Renin; Sodium

To test the hypothesis that elevated atrial natriuretic peptide (ANP) may be involved in altered fluid homeostasis at high altitude, we examined 25 mountaineers at an altitude of 550 m and 6, 18, and 42 h after arrival at an altitude of 4,559 m, which was climbed in 24 h starting from 3,220 m. In 14 subjects, symptoms of acute mountain sickness (AMS) were absent or mild (group A), whereas 11 subjects had severe AMS (group B). Fluid intake was similar in both groups. In group B, urine flow decreased from 61 +/- 8 (base line) to 36 +/- 3 (SE) ml/h (maximal decrease) (P less than 0.05) and sodium excretion from 7.9 +/- 0.9 to 4.6 +/- 0.7) mmol.l-1.h-1 (P less than 0.05); ANP increased from 31 +/- 4 to 87 +/- 26 pmol/l (P less than 0.001), plasma aldosterone from 191 +/- 27 to 283 +/- 55 pmol/l (P less than 0.01 compared with group A), and antidiuretic hormone (ADH) from 1.0 +/- 0.1 to 2.9 +/- 1.2 pmol/l (P = 0.08 compared with group A). These variables did not change significantly in group A, with the exception of a decrease in plasma aldosterone from 189 +/- 19 to 111 +/- 17 pmol/l (P less than 0.01). There were no measurable effects of elevated ANP on natriuresis, cortisol, or blood pressure. The reduced diuresis in AMS may be explained by increased plasma aldosterone and ADH overriding the expected renal action of ANP. The significance of elevated ANP in AMS remains to be established.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aldosterone; Altitude Sickness; Atrial Natriuretic Factor; Diuresis; Hormones; Humans; Hypoxia; Male; Middle Aged; Pulmonary Edema; Water-Electrolyte Balance

Topics: Animals; Atrial Natriuretic Factor; Female; Male; Oleic Acids; Pulmonary Edema; Pulmonary Surfactants; Rats; Rats, Inbred Strains

Protective effect of alpha-human atrial natriuretic peptide (alpha-hANP) on pulmonary edema was investigated using an isolated perfused lung model. Infusion of alpha-hANP (1.7 to 22 ng/ml or 0.56 to 7.3 nM) prevented the edema induced in isolated lung from guinea pig by repeated treatment of 50 micrograms of arachidonic acid at 30 min intervals via the pulmonary artery. The antiedematic action of alpha-hANP was considered to be receptor mediated because the effective concentration was close to the Kd value of the binding of the ANP receptors in the lung homogenate.

Topics: Animals; Arachidonic Acids; Atrial Natriuretic Factor; Guinea Pigs; Humans; In Vitro Techniques; Kinetics; Lung; Male; Pulmonary Edema

Recently, the concept of an atrial endocrine system has expanded to that of a cardiac endocrine system. In support of this expanded view, the cardiac ventricles have been demonstrated to be a source of the atrial hormone (atriopeptin). Markedly enhanced ventricular expression of atriopeptin has been shown to be associated with cardiac hypertrophy. In this study, we measured the levels of atriopeptin in atrial and extra-atrial tissues of the BIO 14.6 hamster, a genetic model of cardiomyopathy and congestive heart failure. The BIO 14.6 hamsters (approximately 1 year of age) weighed 7.4% more than their age-matched controls, an indication of edema, and showed overt cardiac hypertrophy (control vs. BIO 14.6 heart weight: .556 +/- .045 g vs. .990 +/- .043 g). A survey of extra-atrial tissues indicated that pulmonary and ventricular tissue from both control and BIO 14.6 hamsters possessed measurable levels of immunoreactive atriopeptin. However, a comparison of atriopeptin levels in the lungs and cardiac ventricles, respectively, of control and BIO 14.6 hamsters revealed profound differences. Pulmonary atriopeptin levels were 30-fold greater, and ventricular atriopeptin levels were 13.3-fold greater, in the BIO 14.6 hamsters. In addition, the total content of atriopeptin was 2.2-fold greater in the atria of BIO 14.6 hamsters. Dot blot analysis indicated that atriopeptin mRNA levels were greater in the atria (3.4-fold) and ventricles (17.9-fold) of BIO 14.6 hamsters. A similar analysis of atriopeptin mRNA in pulmonary tissue proved inconclusive. The function of the marked increase of pulmonary and ventricular atriopeptin is unknown; however, it is plausible that the peptide hormone serves to regulate the formation of pulmonary and peripheral edema.

Topics: Animals; Atrial Natriuretic Factor; Cardiomyopathy, Dilated; Cricetinae; Heart Atria; Heart Failure; Heart Ventricles; Lung; Pulmonary Edema; RNA, Messenger; Tissue Distribution