atrial-natriuretic-factor and Edema

Body fluid volume regulation by the kidney relies upon the complex interaction of numerous factors. However, in edematous disorders, extrarenal factors can override the 'innate wisdom' of the kidney. For example, in patients with cardiac failure or liver disease and in pregnant women, the normal kidney continues to retain sodium and water despite expanded blood, plasma and extracellular fluid volumes. Such fluid retention can ultimately lead to pulmonary congestion, ascites or peripheral edema. Understanding the kidney's modulation of total body sodium and water in these patients has been perplexing. Cardiac output cannot provide the sole afferent signal for the kidney to regulate sodium and water balance, as the normal kidney can retain excessive amounts of sodium and water when cardiac output is low (e.g. in low output cardiac failure) or high (e.g. cirrhosis or pregnancy). Therefore the integrity of the arterial circulation, which can be impaired either by a low cardiac output or arterial vasodilation, is an important factor in body fluid composition and volume regulation in health and disease.

Topics: Atrial Natriuretic Factor; Cardiac Output, Low; Edema; Female; Humans; Kidney; Myocardial Infarction; Pregnancy; Sodium

Sodium balance in patients with renal failure varies with the severity and clinical manifestations of renal disease. Progressive chronic renal insufficiency is typified by an adaptive increase in the sodium excretion rate per nephron as the total glomerular filtration rate declines. This increase is caused, at least in part, by the effect of atrial natriuretic peptide and other natriuretic peptides, whose release is augmented in the setting of volume expansion and renal failure. However, exogenous administration of natriuretic peptides in clinical chronic and acute renal disease does not consistently increase renal sodium excretion. As the glomerular filtration rate progressively declines towards end-stage renal disease, total renal sodium excretion eventually decreases, and extracellular volume expansion, hypertension, and edema develop. Sodium removal, induced by high dose diuretics or via convective ultrafiltration during dialysis, is necessary to decrease the extracellular volume to normal.

Topics: Acute Kidney Injury; Animals; Atrial Natriuretic Factor; Diuretics; Edema; Glomerular Filtration Rate; Humans; Hypertension; Kidney Failure, Chronic; Renal Dialysis; Sodium

The natriuretic peptide system, which comprises at least four related proteins: atrial natriuretic peptide; brain natriuretic peptide; C-type natriuretic peptide; and urodilatin, exerts important influences on central and renal hemodynamics and renal sodium excretion. Recent studies have examined the role of these peptides in the pathophysiology of edema formation in congestive heart failure, cirrhosis, and nephrotic syndrome and have explored the therapeutic value of manipulating their metabolic pathways. One striking feature appears common to all three states ie, a blunted response to the natriuretic effect of atrial natriuretic peptide, which becomes particularly severe in the late stages of each disease. However, whereas in congestive heart failure and cirrhosis the main mechanism responsible is enhanced proximal tubular reabsorption of sodium resulting in reduced distal sodium delivery to the major site of atrial natriuretic peptide action, in nephrotic syndrome a biochemical defect in the cellular response to atrial natriuretic peptide within the kidney is a more likely explanation. Most information regarding the efficacy of therapies that alter the metabolism or the local action of atrial natriuretic peptide pertain to congestive heart failure. However, continued investigation in this area may ultimately lead to interventions that play a valuable role in the future management of all three edematous states.

Topics: Atrial Natriuretic Factor; Diuretics; Edema; Humans; Natriuresis; Natriuretic Peptide, Brain; Natriuretic Peptide, C-Type; Nerve Tissue Proteins; Peptide Fragments; Peptides; Proteins

In the nephrotic syndrome abnormal sodium and water retention occurs at the kidney level that ultimately causes expansion of interstitial volume and edema. The mechanisms and factors involved remain ill defined. The traditional view has considered hypovolemia, due to urinary protein losses and decreased oncotic pressure, as the afferent stimulus of a complex pathway of responses that come together to enhance reabsorption of sodium and water along the nephron. However, given the fact that only a minority of nephrotic patients have low plasma volume, it has been hypothesized that sodium retention by the kidney is a primary phenomenon occurring in response to intrarenal rather than systemic mechanisms. Experimental evidence is available to support this possibility, and indicates that distal nephron sites are involved in avid sodium retention in the nephrotic syndrome. Several studies have been designed to establish the role of neurohumoral mediators, including the renin-angiotensin-aldosterone axis and sympathetic nervous system. These data suggest that although activation of these systems may contribute to salt retention, they may be minor factors in this process. Recently, attention has focused on atrial natriuretic peptides (ANP), which increase sodium and water excretion in experimental animals and humans. A markedly blunted natriuretic and diuretic response to the systemic infusion of ANP has been reported in the nephrotic syndrome. A defect in the number and affinity of receptor binding sites for the peptide as well as in the level of intracellular cyclic guanosine monophosphate, the second messenger of ANP, has recently been investigated.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Atrial Natriuretic Factor; Edema; Humans; Nephrons; Nephrotic Syndrome; Sodium

The nephrotic syndrome is associated with an expanded interstitial volume and edema due to sodium and water retention. The mechanisms underlying these abnormalities have been only partially clarified. Renal hypoperfusion has been considered the key event that promotes avid sodium and water reabsorption by the kidney. Hypoperfusion results from hypovolemia, a consequence of urinary protein losses and decreased oncotic pressure. However, in some patients plasma volume is normal or even increased, suggesting that in such cases the cause of sodium and water retention might be independent of systemic events and possibly originates in the kidney. Experimental evidence is now available to support this, but the intrarenal mediator(s) that promote the abnormal salt retention are still not fully clear. Atrial natriuretic peptide (ANP), which increases sodium and water excretion, has been suspected to participate in fluid retention. This is consistent with experimental and human data of a markedly blunted natriuretic and diuretic response to systemic infusion of ANP in the nephrotic syndrome. Recent studies of the mechanisms of the blunted natriuretic and diuretic response to ANP documented an increased activity of renal sympathetic nerves, but the results are controversial. The altered response to ANP also may be related to a defect in the number and affinity of receptor-binding sites for the peptide. Evidence also is available of a possible defect at the level of intracellular cyclic guanosine monophosphate, the second messenger of ANP. The gene encoding for a cyclophilin-like protein, which is increased in sodium-retaining conditions, is upregulated in the kidneys of nephrotic rats, and the infusion of ANP further increases cyclophilin-like protein mRNA. Thus, multiple factors probably act in concert to induce edema formation in the nephrotic syndrome. In this review we specifically address the tubular insensitivity to the natriuretic and diuretic action of ANP, which could be an important initiating event and could possibly contribute to sustaining the edema.

Topics: Animals; Atrial Natriuretic Factor; Edema; Humans; Natriuresis; Nephrotic Syndrome

Topics: Animals; Atrial Natriuretic Factor; Cyclic GMP; Edema; Humans; Kidney; Nephrotic Syndrome; Rats; Sodium

This article provides a brief overview of atrial natriuretic factor (ANF). Considered by many investigators to be the putative "third factor" governing sodium excretion, ANF is a peptide actively secreted by the heart, with multiple target organ effectors. As such, ANF represents the first clearly documented cardiac hormone.

Topics: Animals; Atrial Natriuretic Factor; Edema; Heart Failure; Humans; Hypertension; Liver Cirrhosis; Nephrotic Syndrome

It is apparent therefore that a large variety of neurohumoral influences affect renal hemodynamics and the renal tubular reabsorption of sodium and water in response to cardiac failure and thereby contribute to the development of a "salt-avid" kidney, circulatory congestion, and edema formation. These influences are summarized schematically in Figure 1.

Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Edema; Heart Failure; Humans; Kidney; Renin-Angiotensin System; Sodium

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.

Topics: Animals; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Edema; Homeostasis; Hypertension; Rats; Rats, Inbred WKY; Water-Electrolyte Balance

Topics: Amino Acid Sequence; Animals; Atrial Natriuretic Factor; Blood Proteins; Cardenolides; Cattle; Digoxin; Dogs; Edema; Guinea Pigs; Humans; Hypertension; Hypothalamus; Kidney Failure, Chronic; Kidney Tubules; Muscle Proteins; Potassium; Rabbits; Saponins; Sodium; Sodium-Potassium-Exchanging ATPase

The effects of anaritide, a 25-amino-acid synthetic analogue of ANP, were evaluated in 28 patients with cirrhosis complicated by ascites and/or edema. Each patient received two doses of the agent, as well as an infusion of placebo. Six different doses were tested ranging from 0.015-0.300 microgram/kg/min. The infusions lasted for 2 hours and were flanked by both baseline and recovery periods. There was a significant effect of placebo on urinary sodium and chloride excretion rates but no effect on urine flow rate. In response to anaritide, the urine flow rate increased at 0.03, 0.06, 0.075, and 0.100 microgram/kg/min. The sodium and chloride excretion rates increased at all doses except the highest dose. There was no definite effect of anaritide on urinary potassium, calcium, and phosphate excretion rates. There was also no significant effect on creatinine clearance. The mean arterial pressure decreased in response to the 0.060, 0.075, and 0.100 microgram/kg/min doses. In addition, five of the patients receiving the highest dose (0.300 microgram/kg/min) had decreases in their systolic pressures to 90 mm Hg or less. In conclusion, anaritide is natriuretic and diuretic in patients with cirrhosis complicated by ascites and/or edema. Its effect, however, on arterial pressure may limit its therapeutic potential in this patient population.

Topics: Atrial Natriuretic Factor; Blood Pressure; Calcium; Chlorides; Diuresis; Diuretics; Edema; Female; Hematocrit; Humans; Liver Cirrhosis; Magnesium; Male; Middle Aged; Natriuresis; Peptide Fragments; Phosphates; Potassium

Because the role of systemic hormones in the pathophysiology of edema in acute renal disease remains incompletely understood, we compared the levels of atrial natriuretic factor (ANF) and plasma renin activity (PRA) in patients with acute glomerulonephritis (AGN), nephrotic syndrome (NS), and normal individuals during salt deprivation and salt loading. Sixteen patients with AGN (10 males) and nine patients with NS and hypoalbuminemia (7 males) were studied on admission, and after recovery (12 AGN patients) or remission (4 NS patients). Eighteen normal controls were each studied after five days on a low (20 mEq Na/day), regular (120 mEq Na/day) and high (300 mEq Na/day) dietary salt intake. Patients with AGN and NS had comparable edema (AGN 2.8 +/- 0.53 kg; NS 3.36 +/- 0.47 kg; SE) and urinary Na excretion (mean +/- SEM: AGN 0.97 +/- 0.11 mEq/hr; NS 1.06 +/- 0.16 mEq/hr), but AGN patients had five times higher ANF (AGN 27.2 +/- 4.06 fmol/ml; NS 5.51 +/- 1.02 fmol/ml; P less than 0.001) and six times lower PRA ng/liter.sec levels (AGN 0.187 +/- 0.047; NS 1.144 +/- 0.222; P less than 0.001) than NS patients. The degree of edema was correlated with ANF levels in AGN patients (P less than 0.001) but not in NS patients. There was a strong exponential negative correlation (r = -0.773, P less than 0.0001) between ANF and PRA, in which AGN patients and Na-restricted controls were located in the opposite ends of the volume sensing-response, and NS patients in the middle, alongside controls with regular Na intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Adolescent; Atrial Natriuretic Factor; Child; Diet, Sodium-Restricted; Edema; Female; Glomerulonephritis; Humans; Male; Natriuresis; Nephrotic Syndrome; Renin; Sodium, Dietary

This study aimed to evaluate available volume status assessment tools in nephrotic syndrome (NS). Sixty children with INS were subdivided into hypovolemic and nonhypovolemic groups based on fractional excretion of sodium (FeNa%); all were studied for inferior vena cava collapsibility index (IVCCI), plasma atrial natriuretic peptide (ANP), and body composition monitor (BCM). Forty-four patients had nonhypovolemic and 16 had hypovolemic states. ANP did not differ between both groups. IVCCI was higher in hypovolemic group (p < 0.001) with sensitivity 87.5% and specificity 81.8% for hypovolemia detection, while BCM overhydration (BCM-OH) values were higher in nonhypovolemic group (p = 0.04) with sensitivity = 68.2% and specificity = 75% for detection of hypervolemia. FeNa% showed negative correlation with IVCCI (r =  -0.578, p < 0.001) and positive correlation with BCM-OH (r = 0.33, p = 0.018), while FeNa% showed nonsignificant correlation to ANP concentration. IVCCI is a reliable tool for evaluating volume status in NS and is superior to BCM.

Topics: Atrial Natriuretic Factor; Child; Edema; Humans; Hypovolemia; Nephrotic Syndrome; Sodium; Ultrasonography; Vena Cava, Inferior

Previously reported ideal target mean arterial pressure (MAP) after control of bleeding in traumatic hemorrhagic shock (THS) requires further verification in more clinically related models. The authors explored this issue via gradient volume loading without vasopressor therapy. As certain volume loading can induce secretion of atrial natriuretic peptide (ANP), which has been shown to be protective, the authors also observed its potential role.. Fifty male New Zealand rabbits were submitted to 1.5 h of uncontrolled THS (with another eight rabbits assigned to the sham group). After bleeding control, treated rabbits were randomly (n = 10, respectively) resuscitated with blood and Ringer lactate (1:2) to achieve target MAP of 50, 60, 70, 80, and 90 mm Hg within 1 h. During the following 2 h, they were resuscitated toward baseline MAP. Rabbits were observed until 7 h.. After resuscitation, infused fluid was lower and oxidative stress injury was milder in the 70 mm Hg group. Fluid volume loaded during the initial hour after hemostasis was negatively correlated with pH, oxygen saturation, and base excess at the end of resuscitation. It also correlated positively with proinflammatory responses in bronchoalveolar lavage fluid at 7 h and 7-h mortality. Moreover, after volume loading, the 80 mm Hg group showed significantly increased serum ANP level, which correlated with the expression of Akt protein in the jejunum at 7 h.. In rabbits the ideal target MAP during the initial resuscitation of severe THS after hemostasis was 70 mm Hg. ANP may have a critical role in gut protection.

Topics: Animals; Atrial Natriuretic Factor; Blood Pressure; Bronchoalveolar Lavage Fluid; Cytokines; Edema; Fluid Therapy; Hemodynamics; Male; Oxidative Stress; Proto-Oncogene Proteins c-akt; Rabbits; Random Allocation; Resuscitation; Shock, Hemorrhagic; Water-Electrolyte Balance

The natriuretic/diuretic response to atrial natriuretic peptide (ANP), an important regulator of water and Na(+) balance, is markedly attenuated in nephrotic syndrome (NS). It has been suggested that the diminished renal responsiveness to ANP may contribute to the pathogenesis of salt retention and edema formation in NS. However, the mechanisms underlying the renal hyporesponsiveness to ANP remain largely unknown.. The acute effects of exogenous infusion of ANP (5 µg/kg + 10 µg/kg/h) were studied by clearance methodology in control rats, hypoalbuminemic rats with Adriamycin (ADR)-induced NS and in ADR-treated rats infused with hyperoncotic albumin sufficient to restore plasma albumin to normal levels.. Administration of ANP to control rats resulted in a significant increase in urinary flow rate, absolute rate of sodium excretion (+456%) and glomerular filtration rate (GFR). Mean arterial blood pressure decreased following infusion of the peptide. In the nephrotic rats, baseline GFR and Na(+) excretion were significantly lower than in the control animals, and the renal effects of ANP were markedly blunt compared to the control animals. In contrast, the hypotensive effect of ANP in the ADR-treated rats was largely preserved. Infusion of hyperoncotic albumin prior to ANP administration reversed the decrease in baseline GFR and Na(+) excretion and completely restored the renal effects of ANP in the nephrotic rats.. These findings indicate that renal hyporesponsiveness to ANP in rats with ADR-induced NS is a reversible phenomenon that appears to be of functional origin rather than reflecting permanent cellular damage.

Topics: Albumins; Animals; Atrial Natriuretic Factor; Blood Pressure; Disease Models, Animal; Doxorubicin; Edema; Glomerular Filtration Rate; Humans; Hypotension; Inulin; Kidney; Male; Natriuresis; Nephrosis; Nephrotic Syndrome; Rats; Rats, Sprague-Dawley; Renal Circulation; Renin; Salts; Sodium

Low free triiodothyronine (fT3) has been associated with the presence of malnutrition-inflammation syndrome in patients with end-stage renal disease (ESRD) and decreased overall survival in ESRD. Since thyroid hormone has a particular effect on body fluid status, we hypothesized that hemodialysis patients with low-T3 syndrome might have interstitial edema. In this study, we examined the relationship between levels of thyroid hormone and body composition parameters in Japanese hemodialysis patients.. The subjects were 52 patients on maintenance hemodialysis. Serum levels of thyroid hormone and atrial natriuretic peptide (hANP) were measured. Body composition parameters were measured using a bioimpedance body composition analyzer.. Serum fT3 had positive correlations with body mass index (BMI), body fat mass (BFM), total body water (TBW) and intracellular water (ICW), and negative correlations with the ratio of extracellular water to total body water (ECW/TBW) and hANP. There were no correlations between serum fT4 and any body composition parameter. The 49 patients with data at baseline and after 1 year were divided into groups with increased (n = 33) and decreased (n = 16) fT3 after 1 year. ΔBMI and ΔBFM were significantly lower and ΔTBW, ΔICW, ΔECW and ΔECW/TBW (changes over 1 year from baseline) were significantly higher in patients with decreased fT3 compared to those with increased fT3. There was no significant difference in ΔhANP or Δcardiothoracic ratio between the two groups.. These results show that a decrease in fT3 might be associated with emaciation and interstitial edema in Japanese hemodialysis patients.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Body Composition; Body Fluids; Body Mass Index; Body Water; Edema; Emaciation; Female; Humans; Intracellular Fluid; Japan; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Retrospective Studies; Thyroxine; Triiodothyronine

The pathogenesis of edema in nephrotic syndrome is not entirely understood. The aim of this study was to contribute to the discussion on edema pathogenesis in nephrotic syndrome by following changes in volume and sodium retention for the course of the disease in children with steroid-sensitive nephrotic syndrome (SSNS).. Forty-one children with SSNS were included in the study. The patients were divided into three groups (group I: relapse-edematous; group II: relapse-edema free; group III: remission). We investigated the value of the significance and area of sodium retention and vasoactive hormones. In addition, we measured parameters such as inferior vena cava collapsibility index, left atrium diameter, and total body water (TBW) to determine the volume load and cause of edema in children with SSNS.. TBW increased in the relapse-nephrotic syndrome group and the difference was statistically significant among groups (P < 0.001). However, inferior vena cava collapsibility index and left atrium diameter were not different among groups. Fractional sodium excretion was lower in children with relapse nephrotic syndrome (P < 0.05).. Although TBW increases in children with SSNS, intravascular volume is normal. In addition, hypoalbuminemia and sodium retention of the proximal tubule cause edema in children with SSNS.

Topics: Albumins; Aldosterone; Atrial Natriuretic Factor; Blood Volume; Body Water; Child; Child, Preschool; Echocardiography, Doppler, Color; Edema; Female; Heart Atria; Humans; Male; Nephrotic Syndrome; Recurrence; Renin; Sodium; Vena Cava, Inferior

Pioglitazone is an insulin-sensitizer with a thiazolidinedione structure. It is used to reduce hyperglycemia and is frequently prescribed to type 2 diabetic patients. However, it causes edema as an adverse effect in some patients. Although the mechanism of edema is unclear, it may bring an increased risk of congestive heart failure. We investigated whether pioglitazone correlates with the level of plasma human atrial natriuretic peptide (hANP), a marker for congestive heart failure. We administered 15 mg/day of pioglitazone for 3 months to 49 patients (34 men and 15 women; mean age: 64+/-12 years) with type 2 diabetes and no history of pretibial edema. Three of the patients complained of pretibial edema during the 3-month period, and their plasma hANP levels were higher than those of the other 46 before and during the treatment. We therefore suspect that pretibial edema appearing after administration of low-doses of pioglitazone coincides with the level of plasma hANP, and that the appearance of pretibial edema may reflect an increase in circulating blood volume induced by pioglitazone.

Topics: Aged; Aged, 80 and over; Atrial Natriuretic Factor; Diabetes Mellitus, Type 2; Edema; Female; Humans; Hypoglycemic Agents; Male; Middle Aged; Pioglitazone; Thiazolidinediones; Tibia

To identify and localize hyaluronan (HYA) and alpha-atrial natriuretic polypeptide (ANP) in human nasal polyps and to measure the HYA concentrations.. Twelve nasal polyps were collected during routine polypectomies and processed histochemically and biochemically to determine the occurrence of HYA. The distribution of ANP was investigated using an immunocytochemical method.. HYA was unevenly distributed, being found abundantly in the surface epithelium and basement membrane and around fibres and vessels in the lamina propria. It was also present around seromucinous glands and in the secretion of cysts in the stroma. The HYA concentration was 1,000-fold higher than in serum. ANP was abundant in the apical part of ciliated surface epithelial cells and extracellularly in the basement membrane. In the stroma, ANP was confined to apical acinar cells of the seromucinous glands.. Osmotically active HYA and numerous ANP-immunoreactive cells, active in fluid and/or ion transport functions, are present in human nasal polyps. These substances may well be involved in oedema formation and the successive growth of nasal polyps. The high concentrations of HYA in nasal polyps may be of clinical significance for the future development of a local enzyme treatment for nasal polyposis.

Topics: Adult; Atrial Natriuretic Factor; Basement Membrane; Edema; Epithelial Cells; Female; Humans; Hyaluronic Acid; Immunohistochemistry; Male; Middle Aged; Nasal Mucosa; Nasal Polyps; Stromal Cells

Topics: Atrial Natriuretic Factor; Cardiomyopathy, Restrictive; Child, Preschool; Diagnosis, Differential; Diagnostic Imaging; Edema; Humans; Male; Pericarditis, Constrictive

Topics: Adult; Atrial Natriuretic Factor; Body Weight; Edema; Female; Humans; Renin

To study the regulation of antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) in obese and lean women with a swelling syndrome.. Thirty-four obese women and 12 lean women with a swelling syndrome and an abnormal isotopic test of capillary permeability to albumin were investigated.. After 10 nocturnal hours of fluid restriction, subjects were asked at 8am to ingest a tap water load of 20 ml/kg within 10 min and to remain strictly recumbent until twelve noon on the first day, and to remain standing and to walk around until twelve noon on the second day. Free water clearance and the cGMP/creatinine and albumin/creatinine ratios were determined hourly in the morning.. The total 4 h-urinary volume/ingested water volume ratio was significantly lower on the second day both in the lean and the obese patients, the differences being slightly larger in the obese patients. The increase in free water clearance was significantly less on the second day in the obese patients. The increase in cGMP/creatinine ratio was also significantly lower on the second day in the obese patients. The maximum level of the urinary albumin/creatinine ratio was significantly higher on the second day in the obese patients.. In obese women with a swelling syndrome: (1) The higher increase in the urinary albumin excretion rate after water loading followed by a sustained upright position suggests a widespread alteration in capillary function, which is also indicated by the isotopic test of capillary permeability to albumin. (2) The water load-induced inhibition of ADH secretion and stimulation of ANP secretion or ANP activity, more defective in the upright position than in the recumbent one, is probably another major contributing factor to orthostatic oedema.

Topics: Adult; Albumins; Atrial Natriuretic Factor; Capillary Permeability; Case-Control Studies; Creatinine; Drinking; Edema; Female; Guanosine Monophosphate; Humans; Middle Aged; Obesity; Posture; Statistics, Nonparametric; Vasopressins

We examined the response to hypertonic saline challenge (SC) as a potential predictor of fluid retention during heart failure induced by rapid ventricular pacing.. Twelve dogs (22 +/- 4 kg) were given an intra-arterial bolus of 30 ml of 20% saline after establishing baseline fluid intake and urine output (24 h). Dogs were classified according to whether they drank more (Group A) or less (Group B) than the amount required to dilute the s.c. to isotonicity. Fluid retention was then assessed during heart failure after rapid ventricular pacing according to a graded ordinal scale and correlated with the responses to s.c... No difference was noted in baseline fluid intake (1112 +/- 236 ml in Group A vs. 809 +/- 129 ml in Group B). Five hours after s.c. cumulative water intake was significantly greater in Group A than in Group B (1018 +/- 136 vs. 591 +/- 17 ml) (P < 0.01). Urine sodium concentration was 113 +/- 11 and 124 +/- 28 mmol/l at baseline in Group A and B, respectively; increased to 190 +/- 21 and 295 +/- 59 mmol/l at 5 h and remained elevated 24 h after s.c., 177 +/- 60 and 274 +/- 55 mmol/l (both P < 0.01 for within-group comparisons vs. baseline). Urine sodium concentration was less in Group A than in Group B at 5 and 24 h (P < 0.05). The fluid retention score was greater in Group A (3.6 +/- 0.5) than in Group B (0.8 +/- 0.4) (P < 0.01). Fluid retention in heart failure correlated with water intake after the pre-pacing s.c. (r = 0.68, P < 0.025) and inversely with urine concentrating ability (r = -0.58, P < 0.05). Furthermore, water intake and urine concentrating ability following the s.c. were inversely related (r = -0.67, P < 0.02).. We conclude that normal dogs may be classified according to their fluid intake after s.c.. Those dogs that drank excessively and produced a dilute urine were more likely to retain fluid during pacing-induced heart failure. Hence, fluid intake and the ability to excrete a concentrated urine after a saline challenge may be useful variables to predict fluid retention in pacing-induced heart failure.

Topics: Animals; Atrial Natriuretic Factor; Cardiac Pacing, Artificial; Dogs; Drinking; Edema; Heart Failure; Kidney Concentrating Ability; Male; Prognosis; Saline Solution, Hypertonic; Sodium; Time Factors

Topics: Adolescent; Aldosterone; Atrial Natriuretic Factor; Blood Volume; Child; Child, Preschool; Disease Progression; Edema; Humans; Kidney Function Tests; Nephrotic Syndrome; Osmotic Pressure; Remission, Spontaneous; Renin; Serum Albumin; Sodium

The aim of this study was to investigate the haemodynamic and endocrinological effects of noninvasive positive pressure ventilation (NIPPV). Eleven patients with oedema and recent hypercapnic and hypoxaemic worsening of a chronic respiratory insufficiency were included. Echocardiography, cardiac radionuclide assessment, blood catecholamines, salt and water handling hormones were measured at admission and discharge (long study (LS)). To discriminate between the action of NIPPV and other treatments, measurements were performed on the fourth day, for 4 h without NIPPV and 4 h with NIPPV (short study (SS)). NIPPV entailed a correction of P(a,CO2) and an increase of P(a,O2) in LS and SS. Oedema disappeared. Body weight decreased (from 85+/-42 to 81+/-40 kg) during LS. Systolic and mean pulmonary arterial pressure decreased in LS and SS. Right ventricular ejection fraction increased in LS. Left ventricular ejection fraction did not change. Cardiac index was normal on admission and then decreased. Natriuretic peptides and catecholamines were increased on admission, whereas plasma renin activity, aldosterone and vasopressin were normal. We suggest that in these patients, oedema can occur independently of renin-angiotensin-aldosterone-vasopressin and with a normal cardiac output. Noninvasive positive pressure ventilation allowed a correction of blood gases, associated with the resolution of oedema, a decrease in pulmonary arterial pressures and an increase in right ventricular ejection fraction.

Topics: Atrial Natriuretic Factor; Body Composition; Case-Control Studies; Edema; Female; Hemodynamics; Hormones; Humans; Hypercapnia; Intermittent Positive-Pressure Ventilation; Male; Middle Aged; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Pulmonary Wedge Pressure; Respiratory Insufficiency; Ventricular Function, Right; Water-Electrolyte Balance

Some patients with chronic obstructive pulmonary disease (COPD) develop oedematous COPD (oCOPD) with peripheral oedema and have a poor prognosis. The cause of the fluid retention is poorly understood but could be due to defective release of a natriuretic factor. We investigated this hypothesis by measuring levels of brain natriuretic peptide (BNP) and atrial natriuretic peptide (ANP) before and after a 0.1 ml/kg/min 2.7% saline infusion in 6 patients with hypoxemic COPD but no history of oedema and 7 COPD patients with oCOPD. Vasopressin, aldosterone, plasma and urinary urea and electrolytes and osmolality were measured. Arterial blood gases and spirometry were also recorded. The two groups were similar in terms of age, weight, PaO2, PaCO2 and FVC. FEV1 was significantly lower in the oCOPD group. The oCOPD group excreted less urine (202 +/- 23 vs. 364 +/- 48 ml; p < 0.05) and less sodium (32 +/- 3 vs. 68 +/- 9 mmol/l; p < 0.01) as a percentage of the saline load given (18 +/- 2 vs. 30 +/- 4%; p < 0.05). Pre-infusion BNP and ANP levels were similar in both groups. BNP and ANP had an exaggerated increase in the oCOPD group on saline loading. In the oCOPD group, ANP levels were significantly greater 1 h after the saline load compared to the pre-infusion values (30 +/- 7 vs. 11 +/- 2; p < 0.05). BNP did not reach significantly greater levels than baseline values until 3 h after the infusion had ended (45 +/- 6 vs. 27 +/- 2; p < 0.05). At 1 h after the saline load, BNP and ANP levels were significantly greater in the oCOPD group (BNP 32 +/- 2 vs. 24 +/- 1; p < 0.01 and ANP 30 +/- 7 vs. 7 +/- 2; p < 0.05) when compared to COPD controls. BNP levels remained significantly different from the COPD control group 3 h after the infusion ended (45 +/- 6 vs. 26 +/- 2; p < 0.05). Although aldosterone levels were greater in the oCOPD group before the saline infusion, the hormone level was suppressed appropriately by the infusion. In conclusion, the cause of oedema in oCOPD and the inability to excrete a saline load is not due to a failure of release of BNP or ANP.

Topics: Aged; Aldosterone; Analysis of Variance; Atrial Natriuretic Factor; Edema; Humans; Lung Diseases, Obstructive; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Prognosis; Sodium; Sodium Chloride

In the isolated perfused rat lung, perfusion with platelet-activating factor causes bronchoconstriction, vasoconstriction and edema formation. The bronchoconstriction and vasoconstriction are largely mediated by thromboxane, whereas the edema formation is due to enhanced vascular permeability unrelated to eicosanoids. Since natriuretic peptides are known to relax smooth muscle and were suggested to attenuate enhanced vascular permeability, we investigated the effect of urodilatin on the PAF-induced alterations in lung function. Pretreatment with urodilatin (0.25 microM or 0.75 microM) reduced the PAF-induced increase in airway and vascular resistance by approximately 50%. Urodilatin pretreatment, however, was completely ineffective against the PAF-induced increase in weight gain and in vascular permeability, as assessed by the vascular filtration coefficient. Furthermore, urodilatin failed to affect the release of thromboxane into the perfusate in PAF-exposed lungs. Thus, urodilatin relaxes airway and vascular smooth muscle, but fails to reduce edema formation in PAF-perfused rat lungs.

Topics: Analysis of Variance; Animals; Atrial Natriuretic Factor; Bronchoconstriction; Bronchodilator Agents; Capillary Permeability; Edema; Female; Lung; Organ Size; Peptide Fragments; Perfusion; Platelet Activating Factor; Rats; Rats, Wistar; Thromboxanes; Vascular Resistance; Vasoconstriction

Plasma Atrial Natriuretic Peptide (ANP) levels are elevated in patients wish chronic obstructive pulmonary disease (COPD) and can play a role in oedema formation. Plasma ANP levels measured in 60 patients with COPD were compared with results of pulmonary haemodynamics, with therapeutic response to treatment in the time of exacerbation of COPD and with physiologic status of patients with stable COPD. Plasma ANP levels did not correlate with right atrial and pulmonary artery pressure, but were significantly related with right ventricular end diastolic volume and with right ventricular wall volume measured by magnetic resonance imaging. Oxygen breathing (2 l/min by nasal prongs in 30 min.) did not change either mean pulmonary artery pressure or ANP levels. Among patients studied during an acute exacerbation of COPD, plasma ANP levels were higher in patients with oedema (302 +/- 185 pg/ml) than in patients without oedema (87 +/- 43 pg/ml). Oxygen therapy applied in one hour did not influence plasma ANP levels. Plasma ANP levels decreased during first three days of treatment in patients with oedema. This decrease was related to the body weight. In the group of patients with hypoxemia in stable COPD, plasma ANP levels (120 +/- 50 pg/ml) were higher in patients with the history of hypercapnia and oedema than in others (54 +/- 15 pg/ml).

Topics: Aged; Atrial Natriuretic Factor; Edema; Humans; Lung Diseases, Obstructive; Middle Aged; Oxygen; Oxygen Inhalation Therapy; Respiratory Function Tests

Plasma levels of atrial natriuretic peptide (ANP) are elevated in patients with chronic obstructive pulmonary disease (COPD) and may have a role in preventing oedema formation in these patients.. Plasma ANP levels were measured in 60 patients with COPD and these measurements were related to pulmonary haemodynamics, response to treatment during exacerbations, and clinical patterns of the stable disease.. Plasma ANP levels did not correlate significantly with right atrial or pulmonary arterial pressures but did correlate significantly with both the right ventricular end diastolic volume and right ventricular wall volume measured by magnetic resonance imaging. Oxygen (2 1/min by nasal prongs for 30 minutes) did not change the mean pulmonary arterial pressure or the level of plasma ANP. In 20 patients with an acute exacerbation of COPD plasma ANP levels were higher in those with oedema (302 (185) pg/ml) than in those without oedema (87 (43) pg/ml). Oxygen given for one hour had no effect on plasma levels of ANP. However, plasma ANP levels fell over the first three days during treatment in those with oedema, the fall correlating with the change in body weight. In a further 20 stable patients with hypoxic COPD, those with hypercapnia and previous episodes of oedema had higher levels of plasma ANP (120 (50) pg/ml) than normocapnic patients with no previous oedema (54 (15) pg/ml).. The level of ANP is high in the plasma of patients with COPD, particularly during exacerbations in those with oedema. The association of a high plasma ANP level and volume overload is shown by the fall in ANP levels with treatment of the oedema, and the correlation between levels of ANP and right ventricular end diastolic or wall volumes.

Topics: Acute Disease; Aged; Atrial Natriuretic Factor; Edema; Forced Expiratory Volume; Hemodynamics; Humans; Lung Diseases, Obstructive; Middle Aged; Oxygen Inhalation Therapy; Pulmonary Circulation; Stroke Volume

Lipoprotein(a) [LP(a)] is an independent risk factor for cardiovascular disease, and it has also been speculated that it promotes thrombosis. Recent studies have shown that patients with gross proteinuria have greatly increased plasma levels of Lp(a), but the genesis is obscure. In the present study, plasma Lp(a) levels were measured in 31 patients with nephrotic syndrome (NS), 24 patients with IgA nephropathy and 43 healthy control subjects. Lp(a) levels were significantly elevated in NS (median 49.0 mg/dl), in contrast to the control subjects and patients with IgA nephropathy (median 7.0 and 9.7 mg/dl, respectively). Plasma Lp(a) levels fell markedly in 10 of 10 NS patients after remission. In NS, Lp(a) levels correlated directly with serum cholesterol levels (P < 0.05) and indirectly with plasma orosomucoid levels (P < 0.05), but not with serum albumin, triglycerides, HDL cholesterol, urinary protein excretion or GFR. In addition, Lp(a) tended to be higher in NS patients with edema (median 54.3 mg/dl) than in patients without edema (19.0 mg/dl; P = 0.06). Nine NS patients were further evaluated with plasma ANP levels and urinary sodium excretion. Plasma Lp(a) correlated directly with ANP (P < 0.01) and indirectly with urinary sodium excretion (P < 0.05). Excellent correlations were found between Lp(a) and VLDL cholesterol and VLDL triglycerides, respectively, suggesting a close link between Lp(a) and triglyceride-rich lipoproteins in nephrosis.

Topics: Adrenal Cortex Hormones; Adult; Atrial Natriuretic Factor; Edema; Female; Humans; Lipids; Lipoprotein(a); Male; Nephrotic Syndrome; Remission Induction

Topics: Animals; Atrial Natriuretic Factor; Blood Pressure; Edema; Glycopeptides; Humans; Hypertension; Natriuresis; Neprilysin; Substrate Specificity; Tissue Distribution

The first human studies using relatively high-doses of ANF revealed similar effects as observed in the preceding animal reports, including effects on systemic vasculature (blood pressure fall, decrease in intravascular volume), renal vasculature (rise in GFR, fall in renal blood flow), renal electrolyte excretion (rises in many electrolytes), and changes in release of a number of different hormones. Whether all these changes are the result of direct ANF effects or secondary to a (single) primary event of the hormone remains to be determined. Certainly, it has been proven that more physiological doses of ANF fail to induce short-term changes in many of these parameters leaving only a rise in hematocrit, natriuresis and an inhibition of the RAAS as important detectable ANF effects in humans. This leads us to hypothesize that ANF is a "natriuretic" hormone with physiological significance. The primary function in humans is to regulate sodium homeostasis in response to changes in intravascular volume (cardiac atrial stretch). Induction of excess renal sodium excretion and extracellular volume shift appear to be the effector mechanisms. The exact mechanism of the natriuresis in humans still needs to be resolved. It appears however, that possibly a small rise in GFR, a reduction in proximal and distal tubular sodium reabsorption, as well as an ensuing medullary washout, are of importance. The pathophysiological role of ANF in human disease is unclear. One may find elevated plasma irANF levels and/or decreased responses to exogenous ANF in some disease states. Whether these findings are secondary to the disease state rather than the cause of the disease remains to be resolved. Therapeutic applications for ANF, or drugs that intervene in its production or receptor-binding, seem to be multiple. Most important could be the antihypertensive effect, although areas such as congestive heart failure, renal failure, liver cirrhosis and the nephrotic syndrome cannot be excluded. Although the data that have been gathered to date allowed us to draw some careful conclusions as to the (patho)physiological role of ANF, the exact place of ANF in sodium homeostatic control must still be better defined. To achieve this, we will need more carefully designed low-dose ANF infusion, as well as ANF-breakdown inhibitor studies. Even more promising, however, is the potential area of studies open to us when ANF-receptor (ant)agonists become available for human use.

Topics: Animals; Atrial Natriuretic Factor; Edema; Humans; Hypertension; Kidney; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface

ANP administered to cirrhotic dogs or chronic caval dogs with ascites and urinary sodium retention (USR) usually causes heterogeneity of natriuretic response. To assess whether this same phenomenon would occur in the absence of edema, ANP at 100 ng/kg/min was given to dogs before and after the induction of USR by a variety of techniques. Eight dogs were over-diuresed with furosemide over a 2-day period, and 9 dogs were subjected to subacute hemorrhage over a similar period. These dogs were retested with ANP one day later. All 8 dogs given furosemide showed no response to ANP (delta UNa V = 7.4 +/- 4.8 microEq/min), compared to a normal response prior to the diuretic (delta UNa V = 128 +/- 34 microEq/min). The 9 hemorrhaged dogs also responded normally to ANP prior to this manipulation (delta UNa V = 74 +/- 14 microEq/min), but a blunted response post-hemorrhage (delta UNa V = 35 +/- 13 microEq/min). This profile was made up of 5 dogs who responded to ANP (delta UNaV = 62 microEq/min) and 4 who had no response whatsoever (delta UNa V = 3 microEq/min). When 8 dogs were given USR because of continuous mineralocorticoid administration, none responded, but all had a magnified natriuretic response to ANP during the 'escape' phase. Eight dogs were administered minoxidil (10 mg) by mouth daily to induce USR. All 8 dogs responded to ANP (delta UNa V = 93 +/- 6 microEq/min) which was no different from the pretreatment response (delta UNa V = 65 +/- 3 microEq/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Atrial Natriuretic Factor; Dogs; Edema; Female; Fludrocortisone; Furosemide; Glomerular Filtration Rate; Hemorrhage; Kidney Diseases; Male; Minoxidil; Natriuresis

To assess the pathophysiological role of endothelin (ET) in the early post-transplantation period, we followed plasma ET concentrations for 2 months from 1 week prior to surgery in four renal transplant patients. Plasma ET concentrations were elevated before transplantation in all patients. In two patients who developed marked pretibial edema, plasma ET concentrations increased before the onset of edema and before the increase in plasma atrial natriuretic peptide (ANP) concentrations, and remained high while the edema persisted. In the other two patients without edema, plasma ET and ANP concentrations fell toward normal immediately after transplantation. Plasma ET concentration increased transiently again in one of these patients when acute rejection occurred. After recovery from this rejection episode, the plasma ET concentration again fell to the normal range. There were significant correlations between plasma ET concentrations and changes in body weight and urine volume. These results suggest that the plasma ET concentration may reflect the function of transplanted kidneys and that ET may modulate body fluid volume regulation after transplantation. In addition, ET may participate in the pathogenesis of acute rejection.

Topics: Adult; Atrial Natriuretic Factor; Body Water; Edema; Endothelins; Female; Humans; Kidney Transplantation; Male; Middle Aged; Renal Dialysis

A 28-year-old woman had hypothalamic disorders (amenorrhea, obesity, psychiatric abnormalities, polydipsia and fever) and chronic glomerulonephritis. She also suffered from general edema associated with cyclical oliguria and polyuria. Her body weight and plasma osmolality increased during the oliguria phase lasting 2 to 8 days and decreased after paroxysmal polyuria accompanied by the natriuresis. These episodes occurred repeatedly, regardless of the treatment with or without diuretics. The release of arginine vasopressin in response to increased plasma osmolality was exaggerated, but changes in plasma volume did not affect arginine vasopressin release. Plasma atrial natriuretic hormone increased in response to a rise in plasma arginine vasopressin and plasma volume during the oliguria phase, thereby resulting in the diuresis and natriuresis. The renin-angiotensin-aldosterone system was secondarily activated by body fluid depletion and diuretics, and this might play an additive role in general swelling. Plasma gonadal hormones did not change to explain the edema. The mechanism of this cyclical edema remains unknown, but it is likely that hypothalamic dysfunction related to psychiatric abnormalities may exaggerate arginine vasopressin release, and enhanced renal sympathetic activity may cause retention of Na and water, and the increase in atrial natriuretic hormone release responding to the plasma volume expansion may bring about the diuresis and natriuresis.

Topics: Adult; Aldosterone; Arginine Vasopressin; Atrial Natriuretic Factor; Body Weight; Chronic Disease; Edema; Female; Follicle Stimulating Hormone; Glomerulonephritis; Growth Hormone; Humans; Hydrocortisone; Hypothalamic Diseases; Luteinizing Hormone; Oliguria; Osmolar Concentration; Plasma; Polyuria; Prolactin; Thyrotropin; Thyroxine; Water-Electrolyte Balance

The pathogenesis of oedema in hypoxic cor pulmonale is poorly understood. One possibility is a failure of atrial natriuretic peptide release, leading to salt and water retention. This hypothesis was tested by observing the response to an intravenous saline challenge in patients with and without cor pulmonale.. Plasma atrial natriuretic peptide concentrations were measured before and for three hours after an intravenous saline load (0.1 ml 2.7% saline/kg/min for 60 minutes) in 20 patients with chronic obstructive airways disease. Ten patients with cor pulmonale, as judged clinically by the presence of peripheral oedema with a previously documented increase in the jugular venous pressure or pleural effusions during an acute exacerbation of airway obstruction (mean (SE) age 67 (3) years, FEV1 0.73 (0.08) 1, arterial oxygen tension (PaO2) 6.4 (0.4) kPa, and arterial carbon dioxide tension (PaCO2) 6.7 (0.3) kPa), were compared with 10 patients with hypoxic chronic obstructive airways disease who had never had oedema (mean age 63 (1) years, FEV1 1.07 (0.09) 1, PaO2 8.6 (0.4) kPa, and PaCO2 5.3 (0.2) kPa). All patients were studied fasting and after diuretics had been stopped for three days. No supplemental oxygen was given.. The mean four hourly urine sodium excretion was less in the patients who had oedema (27 (4.6) mmol, 13% of the intravenous load) than in those without oedema (82 (15.5) mmol, 43% of the load). Initial mean plasma atrial natriuretic peptide values were significantly higher in the patients with cor pulmonale (19.1 (1.6) compared with 10.2 (0.7) pmol/l) and the mean peak rise in atrial natriuretic peptide after the intravenous saline load had been given was 13 (8.0) pmol/l in the patients with cor pulmonale and 5.5 (2.3) pmol/l in the controls. There were no significant differences in plasma and urinary osmolality, blood pressure, or creatinine clearance between the groups.. Patients with chronic obstructive airways disease and cor pulmonale have an impaired ability to excrete a hypertonic intravenous saline load despite a normal physiological release of plasma atrial natriuretic peptide.

Topics: Aged; Atrial Natriuretic Factor; Edema; Humans; Lung Diseases, Obstructive; Middle Aged; Osmolar Concentration; Pulmonary Heart Disease; Sodium Chloride

Two studies were carried out in order to evaluate the plasma atrial natriuretic factor (ANF) concentrations, as well as hemodynamic and renal profiles in a chronic canine model of right heart pressure overload induced by pulmonary artery (PA) banding. In study I (n = 6), the animals were submitted to a gradual increase in pressure to clarify whether an increase in pressure or atrial distension was the main stimulus to ANF secretion. In study II (n = 6), right heart pressure overload was produced more rapidly, resulting in fluid retention and weight gain, thereby completing the model of right heart failure, and allowing an evaluation of the mechanisms involved in ANF resistance. In study I there were significant increases in right atrial pressure over baseline at 20 weeks, ANF levels at 24 weeks and right atrial area at 28 weeks following PA banding. In study II right heart pressures and ANF levels were higher than baseline at 12 weeks (p less than 0.0001), and fluid retention developed between 12-24 weeks in all dogs. The results suggest that increased right heart pressure, rather than atrial size, is a primary stimulus to ANF secretion in chronic right heart pressure overload. Despite the increases in right atrial pressure, clinical fluid retention occurred only with elevations of renin and aldosterone.

Topics: Aldosterone; Animals; Atrial Natriuretic Factor; Blood Pressure; Dogs; Edema; Heart Atria; Hypertension, Pulmonary; Kidney; Kidney Function Tests; Models, Biological; Pulmonary Valve Stenosis; Renin; Sodium, Dietary

Three cases of idiopathic edema are reported with the results of water loading tests. Free water clearance and fractional sodium excretion revealed that three cases were different in water and sodium retention both in supine and upright positions. Aldosterone, plasma renin activity and antidiuretic hormone seemed to little to correspond to water and sodium retention; whereas atrial natriuretic peptide markedly increased in the upright position in all the cases. These data suggest that three cases cannot be explained by a single factor, but that enhanced reduction of venous return to the heart in the upright position may be a common feature in all three cases.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Drinking; Edema; Female; Humans; Posture; Renin; Sodium; Supine Position; Water

The effect of posture on plasma atrial natriuretic hormone (ANH) and renal function was studied in subjects with idiopathic edema. Sixty-five subjects with edema but with no clinical evidence for cardiac, renal, or pulmonary diseases were studied after they had been off all medication for 1 week or more. They had nothing by mouth after midnight and were admitted to the Clinical Research Center at 0800 h. They voided, were weighed, and had their blood pressure and pulse measured in the recumbent and upright positions. A needle was inserted, and subjects were recumbent for 0.5 h, after which blood was drawn for measurement of plasma ANH, serum sodium, potassium, and (in 35 subjects) creatinine. They were then given 150 mL 0.14% sodium chloride solution to drink every 0.5 h for the next 6 h. Urine was collected every 0.5 h for measurement of sodium, potassium, and creatinine. After 4 h of recumbency repeat blood samples were drawn, subjects ambulated for 2 h, after which final repeat blood samples were drawn. Subjects were considered to have postural edema if their upright urinary sodium/previous 2-h urinary sodium was less than 33%, and to have a normal response if it was 33% or more. The clinical characteristics of the 34 patients with postural edema and 31 patients with a normal response were similar. Plasma ANH levels (initial, after oral saline, and after standing) were similar in the two groups, and there was no relationship between changes in ANH and urinary sodium with standing. In conclusion, under conditions of mild oral sodium chloride loading, changes in plasma ANH do not cause the abnormal sodium retention found in patients with postural edema.

Topics: Adult; Atrial Natriuretic Factor; Creatine; Edema; Electrolytes; Female; Glomerular Filtration Rate; Humans; Kidney; Kidney Concentrating Ability; Male; Posture; Sodium Chloride

Low level of plasma atrial natriuretic factor (ANF) under altered dietary sodium and its elevation during bigeminy were found in a 40-year-old woman with idiopathic oedema. The natriuretic effect of this peptide and the role of renin-angiotensin-aldosterone system in oedema formation in this disorder are discussed.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Edema; Female; Humans; Kidney; Radiography; Renin; Sodium; Sodium, Dietary; Urine

Despite intensive investigation, the pathogenesis of sodium retention in patients with chronic liver disease is not fully known. We have studied 19 chronic liver disease patients, 13 without (group 1) and six with (group 2) histories of clinical sodium retention (ascites or edema) by varying dietary sodium intake. The patients were placed on a 20 mmol/day constant diet for 1 wk, followed by a constant 100 mmol/day sodium diet for 1 wk under strict metabolic conditions. After 5 days of equilibration on each diet, blood and urine samples were collected for plasma atrial natriuretic factor levels and urinary sodium excretion. Group 1 patients (n = 6) achieved near sodium balance in 5 days on both a 20-mmol (urinary sodium output = 17 +/- 3 mmol/day) and a 100-mmol sodium diet (urinary sodium output = 80 +/- 5 mmol/day). Atrial natriuretic factor levels in these patients tended to be elevated, but the increase was not significantly greater than that in normal control subjects (10 +/- 4 pg/ml to 19 +/- 4 pg/ml) on the same diets. In contrast, group 2 patients (n = 5) were in significant positive sodium balance on both the 20 mmol/day sodium diet (mean urinary sodium output = 9.5 +/- 3.3 mol/day) and the 100 mmol/day sodium diet (urinary sodium output = 37 +/- 13 mmol/day). This occurred despite significantly elevated baseline atrial natriuretic factor levels and a significant increase in plasma atrial natriuretic factor levels after sodium challenge (62 +/- 9 pg/ml, p less than 0.05) on a 100 mmol/day sodium diet.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Ascites; Atrial Natriuretic Factor; Blood Pressure; Chronic Disease; Edema; Heart Atria; Humans; Hypertension, Portal; Kidney; Liver Cirrhosis; Sodium; Sodium, Dietary; Time Factors

Edema in Parkinson's disease has been considered to be caused by autonomic nervous system dysfunctions, however little is still known about the exact pathophysiological mechanism involved. In this study, we focused on plasma atrial natriuretic peptide (ANP) levels in Parkinson's disease to elucidate the relationship between foot edema and plasma ANP levels. Thirty four cases of Parkinson's disease were studied. Plasma ANP levels were measured using the radioimmunoassay method. The incidence of foot edema in Parkinson's disease was approximately 30% of the cases studied, with a tendency to be more common in patients in the Yahr stages II and III groups. Predilection sites of the edema were observed from the pretibial to dorsal pedis of both lower thighs, especially on the side most severely affected by the disease. Onset of the edema was difficult to clarify because almost all of the patients with foot edema did not notice the edema by themselves. There was no clear relationship between edema and L-DOPA treatment of Parkinson's disease. For treatment of the edema, oral administration of Furosemide was effective in many cases, however the efficacy tended to gradually decrease. Plasma ANP levels in each age group of the Parkinson's disease cases were statistically high when compared to the values of the age-matched normal volunteers. Plasma ANP levels in the patients with foot edema were also significantly high when compared with the edema-free patients (p less than 0.001), however no relationships were found between plasma ANP levels, age and duration of the illness. It is known that plasma ANP is a cardiac hormone with fluid volume-reducing and vasodilating functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aged, 80 and over; Atrial Natriuretic Factor; Autonomic Nervous System Diseases; Edema; Female; Foot Diseases; Humans; Middle Aged; Parkinson Disease

The plasma levels of atrial natriuretic factor (ANF) were measured both during relapse and remission in 8 patients with idiopathic, minimal-lesion nephrotic syndrome. The plasma levels of ANF were significantly higher in the patients during relapse (53.3 +/- 21.2 pg/ml, mean +/- SEM) as compared to the values observed in the same patients during remission (19.4 +/- 4.1 pg/ml; p less than 0.05). This moderate increase in ANF is not likely to be explained by hypervolemia and is associated with sodium and water retention rather than natriuresis and diuresis.

Topics: Atrial Natriuretic Factor; Child; Edema; Female; Humans; Male; Nephrosis, Lipoid; Radioimmunoassay; Recurrence

An increase in central blood volume in microgravity may result in increased plasma levels of atrial natriuretic factor (ANF). Since elevations in plasma ANF are found in clinical syndromes associated with edema, and since space motion sickness induced by microgravity is associated with an increase in central blood volume and facial edema, we determined whether ANF increases capillary permeability to plasma protein. Conscious, bilaterally nephrectomized male rats were infused with either saline, ANF + saline, or hexamethonium + saline over 2 h following bolus injections of 125I-albumin and 14C-dextran of similar molecular size. Blood pressure was monitored and serial determinations of hematocrits were made. Animals infused with 1.0 micrograms.kg-1.min-1 ANF had significantly higher hematocrits than animals infused with saline vehicle. Infusion of ANF increased the extravasation of 125I-albumin, but not 14C-dextran from the intravascular compartment. ANF also induced a depressor response in rats, but the change in blood pressure did not account for changes in capillary permeability to albumin; similar depressor responses induced by hexamethonium were not accompanied by increased extravasation of albumin from the intravascular compartment. ANF may decrease plasma volume by increasing permeability to albumin, and this effect of ANF may account for some of the signs and symptoms of space motion sickness.

Topics: Adaptation, Physiological; Animals; Atrial Natriuretic Factor; Capillary Permeability; Edema; Male; Nephrectomy; Rats; Rats, Inbred Strains; Serum Albumin, Radio-Iodinated; Space Flight; Syndrome

Sodium-retaining cirrhotic and chronic caval dogs with ascites show a heterogeneous natriuretic response to atrial natriuretic factor (ANF) infusions such that half will increase their urinary excretion of sodium and half will show no natriuretic response whatsoever. In these studies we have examined several physiological variables that might discriminate between these two experimental populations. We studied 22 caval dogs (11 natriuretic responders, 11 nonresponders) and 19 cirrhotic dogs (9 responders, 10 nonresponders). After an infusion of rat ANP-(1-28), 125 ng.kg-1.min-1, differences in glomerular filtration rate, blood pressure, or urinary excretion of guanosine 3',5'-cyclic monophosphate (cGMP) could not differentiate between the two types of dogs. When the left kidney of nonresponding dogs in both the caval and cirrhotic groups was either denervated or vasodilated with acetylcholine bromide (60-80 micrograms/min), the attenuation of the natriuretic response to ANF was not reversed. Papillary plasma flow (PPF) after ANF infusion was measured by a Lillienfield technique and averaged 36 +/- 4 ml.min-1.100 g-1 in normal dogs, 10.7 +/- 0.7 ml.min-1.100 g-1 in both responding and nonresponding caval dogs, and 48.3 +/- 1.1 ml.min-1.100 g-1 for each group of cirrhotic dogs. We conclude that differences in renal perfusion, PPF, cGMP generation, or the presence of intact renal nerves cannot explain the lack of a post-ANF natriuretic response in half of caval or cirrhotic dogs. Other physiological determinants must explain the heterogeneity of natriuretic response to ANF observed in edematous dogs.

Topics: Animals; Ascites; Atrial Natriuretic Factor; Blood Pressure; Cyclic GMP; Denervation; Dogs; Drug Resistance; Edema; Female; Fibrosis; Kidney; Ligation; Male; Natriuresis; Renal Circulation; Sodium; Vasodilation; Vena Cava, Inferior

Ingestion of licorice, 100 g daily for 8 weeks, caused a rise in 81% in plasma atrial natriuretic peptide (ANP) concentration in 12 healthy subjects. Mean body weight increment (1.6 kg) correlated with the increase in plasma ANP (r = 0.59; P less than 0.01). The plasma concentrations of antidiuretic hormone, aldosterone, and plasma renin activity decreased. All these hormonal effects, reflecting retention of sodium and fluid volume, were probably due to the known mineralocorticoid properties of licorice. Blood pressure increased transiently and two subjects developed reversible hypertension. The rise in plasma ANP concentration during ingestion of licorice may be considered a physiological response to prevent fluid retention and development of hypertension.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Edema; Female; Glycyrrhiza; Humans; Male; Middle Aged; Plants, Medicinal; Renin-Angiotensin System; Time Factors; Vasopressins

Topics: Atrial Natriuretic Factor; Edema; Female; Furosemide; Glomerular Filtration Rate; Humans; Liver Cirrhosis, Alcoholic; Male; Middle Aged; Natriuresis; Serum Albumin; Water-Electrolyte Balance

The presence and elevation of atrial natriuretic peptide in fetuses has not previously been demonstrated. This study of right atrial pacing in fetal lambs demonstrated a threefold to fourfold increase in atrial natriuretic peptide during the production of fetal hydrops. Its rate of return to a normal level paralleled the clearance of fetal hydrops. Its possible role in fetal cardiovascular hemodynamics is discussed.

Topics: Animals; Atrial Natriuretic Factor; Edema; Female; Fetal Blood; Fetal Diseases; Fetus; Pregnancy; Sheep; Tachycardia

A patient with severe idiopathic edema and long history of diuretic abuse had, in response to salt loading, an inability to increase urinary sodium excretion associated with a paradoxical response (decrease) of urinary dopamine excretion, a non suppressible aldosterone and non stimulable immunoreactive atrial natriuretic factor in plasma. These patterns distinguished this patient from those with a milder form of idiopathic edema who did not abuse diuretics and had, in comparison with controls, marginally decreased urinary sodium and dopamine responses but normal aldosterone suppressibility and ANF stimulability. Since the natriuretic action of ANF appears to be mediated by dopaminergic mechanisms, this severe natriuretic handicap may be due to a chronic diuretic abuse-induced combined ANF and dopamine deficiency.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Dopamine; Edema; Female; Humans; Kinetics; Sodium Chloride

Topics: Animals; Atrial Natriuretic Factor; Edema; Heart Failure; Hemodynamics; Humans

Changes in concentration of human atrial natriuretic peptide (hANP) in normal and toxaemic pregnancy were examined. The maternal plasma concentration of hANP increased gradually during normal pregnancy to a maximum of 20.0 +/- 2.4 pmol/l (mean +/- S.E.M.) after week 36 of pregnancy. From week 20, the plasma concentrations of hANP were significantly higher than those in non-pregnant women (9.3 +/- 2.0 pmol/l). In toxaemia with hypertension, maternal plasma hANP levels were increased after week 26 of pregnancy (37.7 +/- 6.0 pmol/l) compared with those in normal gravida at the same time (17.1 +/- 1.6 pmol/l). Maternal plasma hANP levels in toxaemia only with oedema were not different from those in normal gravida.

Topics: Adult; Atrial Natriuretic Factor; Edema; Female; Humans; Hypertension; Pre-Eclampsia; Pregnancy

Topics: Atrial Natriuretic Factor; Edema; Heart Failure; Humans; Kidney Failure, Chronic; Liver Cirrhosis

The majority of symptoms related to congestive heart failure (CHF) can be derived from the excessive accumulation of fluid in the body. The retention of fluid is the result of the activation of a complex system of compensatory mechanisms working on the kidneys and altering the hemodynamic situation in the body. The compensatory mechanisms are essentially the same as those activated in acute blood loss. The common denominator for CHF and acute blood loss is a decrease of the effective arterial blood volume (EABV), a parameter defined as blood volume in relation to vascular capacity. In the early stages of CHF there is an increased sympathoadrenergic tone, leading to a peripheral vasoconstriction and a decrease of blood flow to the kidneys. Due to a preferential constriction of the efferent arterioles, the filtration fraction is increased and the glomerular filtration rate remains unchanged. However, there is an increased colloid osmotic pressure and a decreased intravascular hydrostatic pressure in the peritubular capillaries. These alterations result in an increased reabsorption of sodium and water in the kidneys. Furthermore, the blood flow in the kidneys is rerouted from the cortical to the juxtamedullary nephrons, which have larger glomeruli and longer loops of Henle. This will further increase the retention of salt and water. The renin-angiotensin-aldosterone (R-A-A) system is also activated due to the decrease of EABV. Angiotensin II exerts about the same effects as norepinephrine--vasoconstriction, rerouting of blood within the kidney and preferential vasoconstriction of the efferent arterioles--all changes contributing to the retention of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Blood Volume; Edema; Extracellular Space; Glomerular Filtration Rate; Heart Failure; Humans; Renal Circulation; Renin-Angiotensin System; Sodium Chloride; Water-Electrolyte Balance

Atrial natriuretic factor (ANF), a recently sequenced cardiac peptide, has been shown to have potent natriuretic, diuretic, and vasodilating effects in several species. We have developed a radioimmunoassay to measure the levels of immunoreactive ANF in human plasma. Plasma levels of ANF in healthy volunteers on a low sodium diet were 9.8 +/- 1.4 pmol/liter and increased to 21.9 +/- 3.0 on a high sodium diet. The levels of atrial natriuretic factor correlated directly with urinary sodium and inversely with plasma renin activity and plasma aldosterone levels. Patients with marked edema due to congestive heart failure had plasma levels of atrial natriuretic factor five times higher than normal (P less than 0.05), whereas patients with cirrhosis and edema had levels that were not different from normal. These results suggest that atrial natriuretic factor plays an important role in the adaptation to increased sodium intake.

Topics: Adult; Aldosterone; Atrial Natriuretic Factor; Diet, Sodium-Restricted; Edema; Heart Failure; Humans; Liver Cirrhosis; Male; Posture; Renin; Sodium; Sodium Chloride; Stroke Volume

The natriuretic action of the atrial natriuretic factor (ANF) was studied in massively proteinuric, anti-natriuretic and edematous nephrotic rats with moderate impairment of renal function. Animals were distributed among four groups: NA----NR, NV----NR, NeA----NR and NA----NeR, where normal atrial (NA) or normal ventricular (NV) or "nephrotic" atrial (NeA) extracts were injected (----) into normal rats (NR) or nephrotic rats (NeR). Control (C) clearance measurements were made before iv injection of the extracts and at four 15-min intervals thereafter (E). Mean arterial pressure and glomerular filtration rate did not change consistently in all four groups from the C to the E period. However, during the first 15-min period after extract injection, statistically significant fractional natriuretic peaks of 332, 361 and 662% of preinjection control values were demonstrable for the NA----NR, NeA----NR and NA----NeR groups, respectively, but not for NV----NR. Following the natriuretic peak, natriuresis returned to control values for NA----NR, but remained above control levels for the NeA----NR and NA----NeR groups. We conclude that, since both the atrial extract from nephrotic rats injected into normal rats and the atrial extract from normal rats injected into nephrotic rats elicited marked natriuresis, the anti-natriuretic edematous condition observed in nephrotic animals cannot be attributed either to the absence of ANF in their atria or to the unresponsiveness of their kidneys to ANF.

Topics: Animals; Atrial Natriuretic Factor; Edema; Glomerular Filtration Rate; Kidney Diseases; Male; Natriuresis; Nephrotic Syndrome; Rats; Rats, Inbred Strains; Sodium