atrial-natriuretic-factor and Polyuria

To review the physiological changes of aging which affect the systems involved in urine formation and to consider how these changes interact with changes in bladder function, thereby leading to the onset of nocturnal polyuria with associated urinary frequency, nocturia, and incontinence. Based on this information, data are presented on the effectiveness of pharmacological interventions which reduce the rate of urine formation and, thus, can be of benefit in reducing symptoms, especially during the nighttime.. Peer-reviewed journal articles were identified by MEDLINE Search and by review of the literature.. As a consequence of age-associated diminished renal concentrating capacity, diminished sodium conserving ability, loss of the circadian rhythm of antidiuretic hormone secretion, decreased secretion of renin-angiotensin-aldosterone, and increased secretion of atrial natriuretic hormone, there is an age-related alteration in the circadian rhythm of water excretion leading to increased nighttime urine production in older people. The interaction of nocturnal polyuria with age-related diminution in functional bladder volume and detrusor instability results in the symptoms of urinary frequency, nocturia and, in some persons, incontinence. The additional impact of Alzheimer's disease on these physiological and aging changes, as well as on a diminished perception of bladder fullness, leads to an even greater risk of urinary incontinence in these patients. Treatment of nocturnal polyuria with the antidiuretic hormone analog, DDAVP (desmopressin), can result in decreased nocturnal urine production with improvement in symptoms of frequency, nocturia, and incontinence.

Topics: Age Factors; Aged; Aging; Arginine Vasopressin; Atrial Natriuretic Factor; Behavior Therapy; Causality; Circadian Rhythm; Deamino Arginine Vasopressin; Humans; Imipramine; Kidney; Polyuria; Renal Agents; Renin-Angiotensin System; Time Factors; Urodynamics

The atria, strategically located at the junction of the venous and arterial circulation, contain a network of neural and humoral structures by which they sense and regulate intravascular volume. Atrial receptors, most commonly consisting of complex unencapsulated nerve endings discharging into myelinated vagal fibers, are located in the intrapericardial portions of the caval and pulmonary veins and the adjacent atrial walls. Receptor activation by atrial distension results in increased afferent vagal fiber discharge, which in turn leads to tachycardia (Bainbridge's reflex) and decreased renal sympathetic nerve activity, renal vasomotor tone, and antidiuretic hormone activity. In addition, atrial distension also releases ANF, a peptide with potent diuretic, natriuretic, and vasorelaxant actions. The combined effect of these neurohumoral changes is the production of a large hypotonic diuresis. In the clinical setting the volume-regulating role of the atria is demonstrated by the tachycardia-polyuria syndrome. Laboratory and clinical evidence points to the activation of atrial neurohumoral mechanisms in response to atrial distension as the mediators of the polyuria that often accompanies paroxysmal tachycardias. The involvement of these mechanisms in other forms of cardiac congestion and the capability to easily measure in the blood an index of atrial distension, namely ANF, provide the opportunity to elucidate the pathophysiology and hence to open new therapeutic avenues in many cardiac disorders.

Topics: Animals; Atrial Natriuretic Factor; Blood Volume; Heart Atria; Humans; Polyuria; Receptors, Atrial Natriuretic Factor; Receptors, Cell Surface; Syndrome; Tachycardia

To demonstrate nocturnal polyuria objectively and to assess the role of atrial natriuretic peptide (ANP) in healthy elderly males with and without nocturnal polyuria (NP).. 31 healthy elderly men known to have NP (passing more than 33% of their 24-hour urine output during an 8-hour period overnight) and 12 controls without NP were invited to take part in the study. Blood and urine samples were collected at 4-hourly intervals in order to measure urine output, serum and urine electrolytes and osmolality as well as serum cortisol, renin, aldosterone, arginine vasopressin (AVP) and ANP.. 26 men with NP and 8 controls agreed to take part in the study. Subjects with NP were found to have a diuresis and natriuresis as well as a significant increase in ANP overnight compared to the control group. There was no difference in the other parameters between the 3 groups, with the exception of aldosterone and AVP.. This study has shown a group of subjects with increased natriuresis and diuresis overnight, associated with an increase in ANP. It is possible that subclinical cardiac failure causes an increase in ANP therefore causing nocturnal urinary symptoms and this theory needs further exploration.

Topics: Aged; Aged, 80 and over; Aldosterone; Analysis of Variance; Atrial Natriuretic Factor; Biomarkers; Circadian Rhythm; Humans; Hydrocortisone; Male; Middle Aged; Polyuria; Radioimmunoassay; Reference Values; Renin; Urinalysis

Polyuria is found in patients with spinal cord injury (SCI). However, the underlying cellular and molecular mechanism is unknown. Here, we show that mice had elevated urine for 7 days after T

Topics: Animals; Atrial Natriuretic Factor; Epithelial Sodium Channels; Female; Humans; Male; Mice; Polyuria; Signal Transduction; Spinal Cord Injuries; Water

To investigate the urodynamic changes in patients with obstructive sleep apnea-hypopnea syndrome (OSAHS) and nocturnal polyuria.. From Sept. 2002 to Jun. 2008, 23 patients with nocturnal polyuria were diagnosed as having OSAHS by polysomnography (PSG). The number and output of nocturia, the osmotic pressure and the excretion of Na(+) were recorded during both the PSG night and CPAP titrating night. Plasma levels of brain natriuretic peptide (BNP) and atrial natriuretic peptides (ANP) were also measured at 11PM in the 2 nights and 7AM in the next mornings. Urodynamic studies including urine flow, bladder pressure during filling, pressure-flow study during voiding and urethral pressure were carried out in these patients. Urodynamic studies were performed again after treatment with CPAP for 3 months.. PSG showed that the patients with nocturnal polyuria had moderate to severe OSAHS, in which the apnea-hypopnea index (AHI) being 48 ± 15 events per hour. The number of nocturnal voiding during the PSG night was more than that during the CPAP titrating night. During the PSG night, the output of nocturia, the nocturia excretion of Na(+), ANP levels (at 7am in the next morning after PSG night) increased and the osmotic pressure of nocturia decreased. CPAP therapy could reverse these abnormalities. The main characteristics of urodynamics in these patients included weak detrusor contraction, hypoesthesia in filling cystometry, and decreased bladder compliance, and detrusor external sphincter dyssynergia. After 3 months of CPAP treatment, both the motility of the detrusor of bladder and the bladder compliance improved.. CPAP therapy can effectively reverse the nocturnal polyuria in OSAHS patients. In OSAHS patients, the features of nocturia, including the changes of output, osmotic pressure and the excretion of Na(+), may be related to the secretion of high-level of ANP. During the course of chronic progressively OSAHS pathophysiology, detrusor function of bladder may be damaged. CPAP therapy could decrease the nocturnal excretion of ANP, and improve the motility of the detrusor of bladder.

Topics: Adult; Aged; Aged, 80 and over; Atrial Natriuretic Factor; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Nocturia; Polyuria; Sleep Apnea, Obstructive; Urinary Bladder; Urodynamics

The transition from day to night is associated with a pronounced decline in diuresis with reductions in the amount of excreted water, electrolytes, and other end products of our metabolism. Failure to do so leads to a large urine output at night, a condition known as nocturnal polyuria, encountered in a large proportion of children with nocturnal enuresis. The aim of this study was to clarify the mechanisms responsible for the nocturnal polyuria seen in enuretics with inadequate response to desmopressin (dDAVP). Forty-six enuretics (7-14 yr of age) and fifteen age-matched controls were admitted for a 24-h protocol with standardized fluid and sodium intake, comprising urine collections, blood sampling, and blood pressure monitoring. We included patients with severe enuresis (5 +/- 1 wet nights/wk) showing <50% reduction in wet nights on dDAVP. We characterized the patients on the basis of their nocturnal urine production. The children with nocturnal polyuria excreted larger amounts of sodium and urea at night than nonpolyurics and controls. Solute-free water reabsorption as well as urinary arginine vasopressin and aquaporin-2 excretion were normal in polyurics, and no differences were found in atrial natriuretic peptide, angiotensin II, aldosterone, and renin levels. Urinary prostaglandin E2 (PGE2) excretion was significantly higher in polyurics. The nocturnal polyuria in children with dDAVP-resistant nocturnal enuresis seems to be the result of augmented sodium and urea excretion. The high urinary PGE2 levels found in these children point toward a role for increased prostaglandin synthesis in the pathogenesis of enuresis-related polyuria.

Topics: Adolescent; Aldosterone; Antidiuretic Agents; Aquaporin 2; Arginine Vasopressin; Atrial Natriuretic Factor; Child; Circadian Rhythm; Deamino Arginine Vasopressin; Dinoprostone; Drinking; Drug Resistance; Female; Humans; Male; Natriuresis; Nocturnal Enuresis; Polyuria; Renin; Sodium; Sodium Chloride, Dietary; Urea

Renal impairment is common in preterm infants, often after exposure to hypoxia/asphyxia or other circulatory disturbances. We examined the hypothesis that this association is mediated by reduced renal blood flow (RBF), using a model of asphyxia induced by complete umbilical cord occlusion for 25 min (n = 13) or sham occlusion (n = 6) in chronically instrumented preterm fetal sheep (104 days, term is 147 days). During asphyxia there was a significant fall in RBF and urine output (UO). After asphyxia, RBF transiently recovered, followed within 30 min by a secondary period of hypoperfusion (P < 0.05). This was mediated by increased renal vascular resistance (RVR, P < 0.05); arterial blood pressure was mildly increased in the first 24 h (P < 0.05). RBF relatively normalized between 3 and 24 h, but hypoperfusion developed again from 24 to 60 h (P < 0.05, analysis of covariance). UO significantly increased to a peak of 249% of baseline between 3 and 12 h (P < 0.05), with increased fractional excretion of sodium, peak 10.5 +/- 1.4 vs. 2.6 +/- 0.6% (P < 0.001). Creatinine clearance returned to normal after 2 h; there was a transient reduction at 48 h to 0.32 +/- 0.02 ml.min(-1).g(-1) (vs. 0.45 +/- 0.04, P < 0.05) corresponding with the time of maximal depression of RBF. No renal injury was seen on histological examination at 72 h. In conclusion, severe asphyxia in the preterm fetus was associated with evolving renal tubular dysfunction, as shown by transient polyuria and natriuresis. Despite a prolonged increase in RVR, there was only a modest effect on glomerular function.

Topics: Algorithms; Animals; Animals, Newborn; Asphyxia; Atrial Natriuretic Factor; Blood Pressure; Creatinine; Female; Fetus; Heart Rate, Fetal; Hemodynamics; Immunohistochemistry; Kidney; Kidney Function Tests; Kidney Glomerulus; Polyuria; Potassium; Pregnancy; Renal Circulation; Renin; Sheep; Sodium; Sodium-Potassium-Exchanging ATPase

To investigate the effect of treatment with continuous positive airway pressure (CPAP) on nocturnal polyuria in patients with obstructive sleep apnea syndrome (OSAS).. 15 patients with obstructive sleep apnea syndrome were included. The number of nocturia, the nocturia output, the osmotic pressure of nocturia and the nocturia excretion of Na(+) were recorded. Plasma levels of atrial natriuretic peptide (ANP) in night were measured in 8 patients. After treatment with CPAP, all the criteria were repeated.. (1) The number of nocturia decreased significantly after treatment with CPAP (P < 0.01); (2) The difference between nocturia output pre-and post treatment was significant (P < 0.01); (3) The osmotic pressure of nocturia rose from (381 +/- 96) mmol/L to (570 +/- 169) mmol/L (P < 0.05); (4) The nocturia excretion of Na(+) dropped from (1.16 +/- 0.35) mmol/h to (0.63 +/- 0.13) mmol/h (P < 0.01); (5) Plasma levels of ANP in night decreased from (146 +/- 14) ng/L to (106 +/- 10) ng/L (P < 0.01); (6) After treatment with CPAP, the reduction of ANP is correlated with the reduction of the nocturia output, the addition of the osmotic pressure of nocturia and the reduction of the nocturia excretion of Na(+). The correlation coefficients were 0.82, 0.84, 0.81 respectively.. Treatment with CPAP can reduce the number of nocturia, the nocturia output and the nocturia excretion of Na(+), increase the osmotic pressure of nocturia. The changes probably relate to the reduction of plasma level of ANP.

Topics: Adult; Atrial Natriuretic Factor; Circadian Rhythm; Humans; Male; Middle Aged; Polyuria; Positive-Pressure Respiration; Sleep Apnea, Obstructive

We report a case of olivopontocerebellar atrophy without sleep apnea syndrome who presented nocturnal polyuria. It is considered that a disturbance in the circadian rhythm for arginine vasopressin secretion due to degeneration of suprachiasmatic nuclei and marked increase in the secretion of atrial natriuretic peptide due to abnormal diurnal variation in blood pressure may be involved in the mechanism of nocturnal polyuria.

Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Circadian Rhythm; Female; Humans; Hydrocortisone; Middle Aged; Olivopontocerebellar Atrophies; Polyuria; Suprachiasmatic Nucleus; Urination Disorders

Patients with paroxysmal supraventricular tachycardia (SVT) may have a polyuria after termination of tachycardia. There is increasing evidence that the renal peptide urodilatin (ANP (95-126))--and not plasma ANP (ANP (99-126))--is the member of the natriuretic peptide family mediating natriuresis and diuresis in man. In patients with SVT we, therefore, analyzed the relationship between diuresis, natriuresis, plasma ANP, urinary urodilatin excretion and renal excretion of cyclic GMP, the second messenger in the ANP system. During and after clinical presentation with spontaneously occurring SVT, two patients with AV-nodal and one patient with atrioventricular reentry tachycardia (heart rate 160 to 200 bpm) were studied. Urinary urodilatin excretion was correlated to diuresis (r = 0.73) and natriuresis (r = 0.93); similarly urinary cyclic GMP excretion was related to diuresis (r = 0.80) and natriuresis (r = 0.87; p < 0.001, respectively). In contrast, there was no significant correlation between plasma ANP concentrations and diuresis (r = 0.28, n.s.) or natriuresis (r = 0.11, n.s.). As an explorative analysis, stepwise multiple linear regression identified urinary urodilatin as the most important contributor to diuresis and natriuresis after SVT. These data on polyuria after spontaneous SVT further support the view that in man urodilatin is the member of the natriuretic peptide family participating in kidney physiology.

Topics: Adult; Atrial Natriuretic Factor; Cyclic GMP; Diuresis; Female; Glomerular Filtration Rate; Humans; Male; Middle Aged; Natriuresis; Peptide Fragments; Polyuria; Regression Analysis; Tachycardia, Paroxysmal; Tachycardia, Supraventricular

The release of atrial natriuretic peptide (ANP) may be stimulated by tachycardia and the evidence from human studies suggests that this is mediated by a rise in atrial pressure. However, animal experiments suggest that tachycardia can by itself increase ANP levels without increasing right atrial pressure (RAP). We report here the case of a healthy volunteer who had supraventricular tachycardia (SVT) whilst participating in a study evaluating the relationship between changes in RAP and changes in ANP. The ANP levels rose following the SVT but there was no rise in RAP, suggesting that heart rate can modulate ANP levels without changes in RAP as has been shown in animal experiments.

Topics: Adult; Atrial Function, Right; Atrial Natriuretic Factor; Humans; Male; Polyuria; Pressure; Tachycardia, Supraventricular

Severe Guillain-Barré syndrome (GBS) usually results in life-threatening autonomic disturbances requiring a close monitoring of the patient in an Intensive Care Unit. Besides dangerous cardiac manifestations, neuroendocrine changes are also reported and could induce electrolytes and fluid balance impairments. Polyuria has been observed in a severe case of GBS occurring in a 16-year-old boy. Consecutive blood samples were obtained for renin, aldosterone, antidiuretic hormone and atrial natriuretic factor measurements. Polyuria in GBS is multifactorial and would be partly due to a dysregulation of osmoreceptors.

Topics: Adolescent; Aldosterone; Atrial Natriuretic Factor; Autonomic Nervous System Diseases; Critical Care; Humans; Male; Natriuresis; Osmolar Concentration; Plasma Exchange; Polyradiculoneuropathy; Polyuria; Renin

Supraventricular tachycardia was induced in 10 patients by programmed cardiac stimulation through esophageal lead. Blood pressure, heart rate, renal function, and hormonal factors were measured before, during, and after tachycardia. The patients were divided into two groups, depending on whether antinatriuresis occurred during tachycardia; one group (n = 5) with antinatriuresis during tachycardia associated with a decrease in blood pressure and the other group (n = 5) with neither antinatriuresis nor changes in blood pressure. The urinary sodium excretion tended to increase after tachycardia only in the latter group. On the other hand, urine volume and free water clearance increased during or after tachycardia in both groups. Plasma levels of atrial natriuretic peptide significantly increased and the urinary vasopressin excretion significantly decreased during tachycardia in both groups. During tachycardia, natriuresis due to atrial natriuretic peptide secretion seems to be hampered by hypotension, but polyuria is preserved despite the fall in blood pressure probably related to suppression of vasopressin release.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Blood Pressure; Female; Hemodynamics; Humans; Kidney; Male; Middle Aged; Natriuresis; Polyuria; Tachycardia, Supraventricular

The mechanism of polyuria associated with paroxysmal supraventricular tachycardia (SVT) was investigated in 8 patients. SVT was induced artificially and sustained for 60 minutes. Urine and blood samples were collected every 30 minutes. During the latter half of SVT, urine flow increased twofold in the control subjects before SVT. Urinary sodium excretion increased significantly (p less than 0.01) within 30 minutes after SVT. Urinary excretion of antidiuretic hormone (ADH) decreased (p less than 0.01) during the latter half of SVT and increased (p less than 0.01) after SVT, respectively. Plasma level of ADH did not change during SVT but increased (p less than 0.05) after SVT. The concentration of plasma atrial natriuretic polypeptide (ANP) increased significantly (p less than 0.05) before SVT ended. Urinary excretion of prostaglandin E2 increased significantly (p less than 0.05) after termination of SVT. The percent changes in the urinary excretion of prostaglandin E2 were correlated (r = 0.713, p less than 0.001) with those of ADH. There was also a correlation (r = 0.6, p less than 0.001) between the percent changes in the urinary excretion of prostaglandin E2 and those of sodium. Their findings suggest that the polyuria during SVT is attributed mainly to the inhibition of ADH release and that the natriuresis after SVT is due not only to the increased ANP but also to the increased renal prostaglandin E2 probably stimulated by ADH.

Topics: Adult; Atrial Natriuretic Factor; Blood Pressure; Dinoprostone; Female; Heart Rate; Humans; Kidney; Male; Middle Aged; Natriuresis; Osmolar Concentration; Polyuria; Tachycardia, Paroxysmal; Tachycardia, Supraventricular; Vasopressins

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

To examine a possible role for atrial natriuretic peptide (ANP) in water and sodium metabolism disturbances associated with abnormal vasopressin (AVP) secretion, we measured plasma ANP concentrations in 15 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) and in 17 patients with central diabetes insipidus (DI). The mean plasma ANP concentration (30.2 +/- 10.4 pmol/L) in SIADH patients who had hyponatremia, plasma hypoosmolality, hyperosmolar urinary compared to plasma sodium levels, and increased plasma AVP levels relative to plasma osmolality was significantly higher than that in normal subjects (12.6 +/- 4.9 pmol/L), although there was a considerable individual variation in plasma ANP ranging from normal to clearly elevated levels (15.1-47.0 pmol/L). When hyponatremia was corrected by water restriction or demeclocycline administration, plasma ANP levels decreased significantly and fell into the normal range (12.5 +/- 4.3 pmol/L). DI patients who complained of polyuria and polydipsia and had hypoosmolar urine, normal or elevated plasma sodium concentrations, and decreased plasma AVP levels relative to plasma osmolality, on the other hand, had a significantly lower mean plasma ANP level (7.6 +/- 2.9 pmol/L) than normal subjects. There was, again, a considerable overlap between plasma ANP levels in individual DI patients (4.2-13.9 pmol/L) and those in normal subjects. Treatment with 1-desamino-8-D-arginine vasopressin resulted in a significant increase in the mean plasma ANP level (18.6 +/- 8.0 pmol/L). There were no significant correlations between plasma ANP and AVP levels in either group of patients. The results indicate that ANP secretion is modulated by changes in plasma volume consequent to abnormal AVP secretion, which may have a pathophysiological significance in maintaining volume homeostasis.

Topics: Adolescent; Adult; Aged; Atrial Natriuretic Factor; Blood Volume; Deamino Arginine Vasopressin; Demeclocycline; Diabetes Insipidus; Female; Humans; Inappropriate ADH Syndrome; Male; Middle Aged; Polyuria; Sodium; Vasopressins; Water-Electrolyte Balance

Cases which present abnormality in water-electrolyte before and after operation of pituitary adenoma are occasionally reported. The authors have encountered a case in which neurological symptoms became aggravated abruptly with pituitary apoplexy after admission, hyponatremia was noted before operation and polyuria, not hypotonic urine was observed after operation. As a result of an endocrinological examination which may have an influence on water-electrolyte (ADH, aldosterone, ANP, etc.) the ADH level in hyponatremia before operation was high at 6.8 pg/ml; so, it was taken as SIADH. According to a study at the time of polyuria after operation, the ADH level was normal at 2.4 pg/ml, the ANP level was abnormally high at 140 pg/ml and the specific gravity of the urine was kept at 1.010 or more. So, polyuria was considered due to abnormally increased content of serum ANP. In polyuria due to abnormally increased content of serum ANP, the osmotic pressure of the urine is maintained relatively well, which is a clinical feature evidently different from diabetes insipidus. After operation for pituitary adenoma, water-electrolyte should be controlled with polyuria due to abnormally increased content of serum ANP in addition to diabetes insipidus taken into consideration.

Topics: Atrial Natriuretic Factor; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Middle Aged; Pituitary Apoplexy; Polyuria; Postoperative Complications; Water-Electrolyte Imbalance

A concomitant diuresis and natriuresis has been reported to occur in 30-50% of patients with paroxysmal supraventricular tachycardia. While the increase of the diuresis may be secondary to an inhibition of vasopressin, the etiology of the natriuresis is presently not well understood. To determine the role of atrial natriuretic peptide (ANP) in the pathogenesis of tachycardia-induced polyuria, we measured ANP levels in two female patients (aged 59 and 68 years) with recurrent episodes of paroxysmal supraventricular tachycardia during such attacks, as well as after conversion to a normal sinus rhythm. In both patients, episodes of supraventricular tachycardia were associated with both a large increase in ANP plasma levels (560 resp. 1.208 pg/ml; normal range: 50 +/- 10 pg/ml) and polyuria. Despite elevated ANP plasma levels, no diuretic and natriuretic response to tachycardia could be observed during episodes of shorter duration, some of which occurred in the older patient studied. After restoration of a normal sinus rhythm, ANP plasma levels decreased to baseline levels (107 resp. 32 pg/ml). The results of this study show that the secretion of ANP is increased during episodes of paroxysmal supraventricular tachycardia, suggesting that ANP might contribute to the pathogenesis of natriuresis and diuresis frequently associated with supraventricular tachycardia.

Topics: Aged; Atrial Natriuretic Factor; Diuresis; Female; Humans; Middle Aged; Natriuresis; Polyuria; Reference Values; Tachycardia, Supraventricular; Time Factors

Topics: Adult; Atrial Natriuretic Factor; Dinoprostone; Female; Humans; Male; Middle Aged; Polyuria; Tachycardia, Supraventricular; Vasopressins

Atrial natriuretic peptide (ANP) is a cardiac hormone originating from atrial cardiocytes. It seems to be involved in the regulatory control of circulating volume and vascular tone. Plasma immunoreactive atrial natriuretic peptide (IrANP) was investigated in 22 patients with paroxysmal supraventricular tachyarrhythmia (16 with atrial fibrillation, 4 with atrial flutter, one with a Wolf-Parkinson-White syndrome (WPW) and one with atrial tachycardia). During the aute attack, IrANP was significantly increased (125.3 +/- 11.4 pmol/l) compared to samples obtained during convalescence (55.9 +/- 4.7 pmol/l). Heart rate (HR) was 144 +/- 4.3 beats/min during the arrhythmia and 75 +/- 2.6 during convalescence. The reduction of IrANP in plasma from the acute attack of tachycardia to follow-up was significantly related to the reduction of HR (p less than 0.05). Irrespective of type of paroxysmal supraventricular tachyarrhythmia, 50% of the patients experienced polyuria during the attack. This symptom was more frequent in younger patients with a shorter duration of tachycardia. Polyuria patients had a higher HR during the attack of supraventricular tachycardia. Even though polyuria was not always found in the patients with the highest IrANP values, the symptom was associated with significantly higher concentrations of IrANP in plasma compared to the non-polyuria group. We conclude that IrANP is increased in plasma during acute attacks of paroxysmal supraventricular tachycardia. Furthermore, the polyuria frequently associated with this condition may partly be due to excess release of ANP from cardiac myocytes.

Topics: Adult; Aged; Atrial Natriuretic Factor; Humans; Middle Aged; Polyuria; Radioimmunoassay; Tachycardia, Paroxysmal; Tachycardia, Supraventricular

Changes in plasma levels of atrial natriuretic peptide (ANP) and arginine vasopressin (AVP) were studied in 8 patients during a 30 min period of induced supraventricular tachycardia (SVT). The mean plasma ANP concentration increased immediately after the onset of SVT, peaked at 30 min and gradually returned to the control level. The mean plasma AVP concentration, on the other hand, was suppressed during SVT and rebounded above the control level in the post-SVT period. In 4 patients, SVT was associated with polyuria and natriuresis. The mean urine volume in these patients increased to 580% of the control and the mean urinary sodium excretion to 278% of the control, respectively. It was concluded that both a stimulation of ANP secretion and an inhibition of AVP release, elicited by an increase in atrial pressure, may be responsible for polyuria and natriuresis associated with SVT.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Cardiac Pacing, Artificial; Electrocardiography; Female; Humans; Male; Middle Aged; Natriuresis; Polyuria; Radioimmunoassay; Tachycardia, Supraventricular; Time Factors

The human atrial natriuretic polypeptide (hANP) concentration in plasma was measured during paroxysmal supraventricular tachycardia provoked in 2 patients with Wolff-Parkinson-White syndrome. A 10- to 20-fold increase in plasma hANP concentration was observed during the tachycardia: from 12 to 291 pg/ml in 1 case and from 14 to 174 pg/ml in the other. Although polyuria was associated with the tachycardia, urinary sodium excretion as well as urinary osmolality were decreased. The urinary arginine vasopressin was appreciably decreased during the tachycardia. These results suggest that hANP released by paroxysmal tachycardia might not act as a natriuretic factor in this range of plasma concentration. Polyuria during paroxysmal tachycardia was attributed mainly to the inhibition of arginine vasopressin release.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Electric Stimulation; Female; Heart; Humans; Male; Middle Aged; Polyuria; Tachycardia, Paroxysmal; Wolff-Parkinson-White Syndrome

Topics: Adult; Aged; Arrhythmias, Cardiac; Atrial Natriuretic Factor; Female; Heart Atria; Humans; Male; Middle Aged; Muscle Proteins; Polyuria

Plasma concentrations of immunoreactive atrial natriuretic peptide (ANP) were low or undetectable in 8 healthy subjects and 9 control patients without cardiac disease, and raised in 17 patients with congestive heart failure (CHF). Highest concentrations were measured in patients with severe CHF. High plasma ANP levels were also found in 2 patients with paroxysmal supraventricular tachycardia and associated transient polyuria. Infusion of synthetic human alpha-ANP, 110-125 micrograms over 30 min, to 3 healthy males resulted in a 2.3-fold increase in natriuresis and diuresis but had no effect on kaliuresis. Plasma levels of renin activity, aldosterone, and antidiuretic hormone did not change significantly. ANP infusion gave plasma ANP levels of the same magnitude as those found in severe CHF; levels returned to baseline within 15 min of stopping the infusion. Thus ANP appears to be a circulating hormone in man, at least in severe CHF and supraventricular tachycardia.

Topics: Adult; Aged; Atrial Natriuretic Factor; Blood Pressure; Female; Heart Failure; Heart Rate; Hormones; Humans; Infusions, Parenteral; Male; Middle Aged; Muscle Proteins; Polyuria; Tachycardia, Paroxysmal

Postobstructive diuresis occurs after relief of bilateral ureteral obstruction despite the persistent decrease in renal cortical perfusion and glomerular filtration rate (GFR). After an initial transient rise in renal blood flow (RBF) during acute ureteral obstruction, tubular damage and progressive vasoconstriction with decreased RBF, especially of medullary perfusion, are observed with chronic obstruction. These are associated with an activation of the renin-angiotensin system and of renal prostaglandin (PG) synthesis with enhanced production of the vasoconstrictor thromboxane A2. Azotemia and extracellular fluid volume (ECFV) expansion result from impaired renal function. Mechanisms of polyuria following relief from bilateral chronic obstruction include enhanced PGE-mediated medullary blood flow, structural and functional tubular damage with decreased sodium reabsorption and (vasopressin-resistant) impaired renal concentrating ability, osmotic diuresis, activation of natriuretic factors following ECFV-expansion, and sometimes iatrogenic excessive fluid replacement. The resulting loss of fluid and electrolytes represents a major hazard in patients after surgical correction of congenital or acquired urinary tract obstruction.

Topics: Animals; Atrial Natriuretic Factor; Diuresis; Extracellular Space; Glomerular Filtration Rate; Hemodynamics; Humans; Hydronephrosis; Kidney Concentrating Ability; Kidney Tubules; Polyuria; Prostaglandins; Renal Circulation; Renin-Angiotensin System; Ureteral Obstruction; Urodynamics; Water-Electrolyte Balance

Neural reflexes from the heart, in particular the atria, are well documented and are involved in sodium and water excretion. Current work also indicates that the atria have an important endocrine function. Atrial peptides, which have been recently characterized and synthesized, may play a significant role in the homeostasis of body fluids.

Topics: Animals; Atrial Function; Atrial Natriuretic Factor; Body Fluids; Dogs; Heart Atria; Hemodynamics; Hormones; Humans; Polyuria; Rats; Receptors, Neurotransmitter; Tachycardia; Urine