atrial-natriuretic-factor and Water-Electrolyte-Imbalance

This review discusses renal sodium handling in heart failure. Increased sodium avidity and tendency to extracellular volume overload, i.e. congestion, are hallmark features of the heart failure syndrome. Particularly in the case of concomitant renal dysfunction, the kidneys often fail to elicit potent natriuresis. Yet, assessment of renal function is generally performed by measuring serum creatinine, which has inherent limitations as a biomarker for the glomerular filtration rate (GFR). Moreover, glomerular filtration only represents part of the nephron's function. Alterations in the fractional reabsorptive rate of sodium are at least equally important in emerging therapy-refractory congestion. Indeed, renal blood flow decreases before the GFR is affected in congestive heart failure. The resulting increased filtration fraction changes Starling forces in peritubular capillaries, which drive sodium reabsorption in the proximal tubules. Congestion further stimulates this process by augmenting renal lymph flow. Consequently, fractional sodium reabsorption in the proximal tubules is significantly increased, limiting sodium delivery to the distal nephron. Orthosympathetic activation probably plays a pivotal role in those deranged intrarenal haemodynamics, which ultimately enhance diuretic resistance, stimulate neurohumoral activation with aldosterone breakthrough, and compromise the counter-regulatory function of natriuretic peptides. Recent evidence even suggests that intrinsic renal derangements might impair natriuresis early on, before clinical congestion or neurohumoral activation are evident. This represents a paradigm shift in heart failure pathophysiology, as it suggests that renal dysfunction-although not by conventional GFR measurements-is driving disease progression. In this respect, a better understanding of renal sodium handling in congestive heart failure is crucial to achieve more tailored decongestive therapy, while preserving renal function.

Topics: Atrial Natriuretic Factor; Diuretics; Glomerular Filtration Rate; Heart Failure; Humans; Kidney; Kidney Glomerulus; Kidney Tubules; Natriuretic Peptide, Brain; Renal Circulation; Renal Insufficiency, Chronic; Sodium; Water-Electrolyte Imbalance

Nocturia is common in older people and it may be bothersome for both patients and carers. It is most commonly related to bladder storage difficulties and nocturnal polyuria. The former results most frequently from an uninhibited overactive bladder. The latter occurs as a consequence of age-associated changes in the circadian rhythm of urine excretion. The management of an overactive bladder includes both behavioural and drug treatment. The management options for nocturnal polyuria include an afternoon diuretic and desmopressin, but caution is required, particularly with the latter, as it can cause significant hyponatraemia.

Topics: Adult; Aged; Aged, 80 and over; Arginine Vasopressin; Atrial Natriuretic Factor; Circadian Rhythm; Humans; Kidney Diseases; Life Style; Male; Middle Aged; Sleep Wake Disorders; Sodium; Urinary Bladder Diseases; Urination Disorders; Vasopressins; Water-Electrolyte Imbalance

Diuretics continue to be a mainstay in patients with CHF. Conventional diuretic therapy is associated, however, with potentially deleterious neurohumoral activation and renal impairment. It is not known to what extent these neurohumoral effects are offset by concurrent therapy with ACE-I, beta-blockers, and other agents. In the past, there was no alternative to conventional diuretic therapy, so their potential for adverse outcome in the long term could not be assessed. Enhancement of the natriuretic peptide system could provide us with a better strategy to treat sodium and water retention. In a unique way, the natriuretic peptides combine several of the beneficial actions of the other diuretics, but without the associated cost. Natriuretic peptides, like conventional diuretics, are natriuretic and diuretic. There are important differences, however. First, unlike conventional diuretics, NPs do not activate RAAS. Activation of this system is associated with progression of CHF. Second, NPs inhibit the sympathetic nervous system, the activation of which is associated with heart failure progression, myocyte necrosis and apoptosis, and arrhythmias. Third, unlike conventional diuretics that lead to a decrease in GFR by reflex mechanisms. NPs maintain or even improve GFR. We now appreciate that some "old" drugs may be beneficial to CHF patients in a new way, as is the case with spironolactone. The survival benefit of this aldosterone antagonist is clear: its usefulness, however, may be more a result of both its antifibrotic actions in addition to its tradional role as a potassium-sparing and natriuretic agent. It is hoped that the SARAs will provide the same survival benefit, but with fewer of the sex-steroid side effects. In addition, AVP-receptor antagonists may become useful tools in the treatment of patients with hyponatremia. Likewise, the A1 AR antagonists may find a role in the CHF armamentarium by providing good diuresis and natriuresis while at the same time maintaining GFR through inhibition of TGF. Many questions remain unanswered, and studies are needed to demonstrate that the positive results seen in basic research translate into improved morbidity and mortality.

Topics: Aldosterone; Antidiuretic Hormone Receptor Antagonists; Atrial Natriuretic Factor; Diuresis; Diuretics; Heart Failure; Humans; Kidney; Mineralocorticoid Receptor Antagonists; Natriuresis; Natriuretic Peptide, Brain; Neprilysin; Purinergic P1 Receptor Antagonists; Sodium Chloride; Water-Electrolyte Imbalance

The incidence of acute renal failure in pregnancy has decreased. This decrease is less marked in developing countries in which resources are more scarce. The clinical diagnosis of acute renal failure is crude due to the variability of clinical signs and the late occurrence of basic biochemical abnormalities. Obstetric and gynaecological diseases are found among the traditional pre-renal, intra-renal and post-renal causes of acute renal failure. The cornerstone of management is the identification of high-risk cases and the prevention of acute renal failure by maintaining intravascular volume. The evidence for the efficacy of other prophylactic medical interventions, such as the use of loop diuretics, mannitol, low-dose dopamine and others, is poor. Management of established acute renal failure includes restoration of intravascular volume, treatment of any reversible causes, especially pregnancy complications such as pre-eclampsia, strict fluid balance and correction of any electrolyte abnormality or metabolic acidosis. Dialysis is a supportive measure until the kidneys recover.

Topics: Acute Kidney Injury; Adult; Atrial Natriuretic Factor; Cardiotonic Agents; Critical Illness; Diuretics, Osmotic; Dopamine; Female; Fluid Therapy; Humans; Mannitol; Oliguria; Pregnancy; Pregnancy Complications; Pregnancy, High-Risk; Prognosis; Renal Dialysis; Water-Electrolyte Imbalance

Normal aging is associated with changes in body composition, thirst perception, renal function, and the hormonal regulatory systems involved in the maintenance of water and sodium balance. The presence of many diseases and drugs common in the elderly can interact with the impaired homeostatic systems to result in clinically significant disturbances of water and sodium with accompanying symptoms, morbidity, and mortality. These disorders, which include dehydration, hypernatremia, hyponatremia, urinary frequency, and urinary incontinence can either be prevented or promptly recognized and appropriately treated by understanding the physiological changes and clinical circumstances which put the elderly person at increased risk for deranged water and sodium balance.

Topics: Aged; Arginine Vasopressin; Atrial Natriuretic Factor; Female; Frail Elderly; Humans; Inappropriate ADH Syndrome; Male; Risk Factors; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Topics: Adrenomedullin; Angiotensin II; Animals; Atrial Natriuretic Factor; Endothelins; Glomerular Filtration Rate; Humans; Kidney Tubules, Proximal; Natriuresis; Nitrous Oxide; Peptides; Renal Circulation; Vasopressins; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Body Weight; Cyclic GMP; Electric Conductivity; Humans; Renal Dialysis; Ultrasonography; Vena Cava, Inferior; Water-Electrolyte Balance; Water-Electrolyte Imbalance

The delicate interplay between vasoconstrictors and vasodilators preserves glomerular filtration in CHF despite marked hypoperfusion. Activation of vasoconstrictive systems seems to depend on the severity and the chronicity of the disease. The importance of renin-angiotensin, sympathetic nerves, vasopressin and counterregulatory ANP, and prostaglandins in CHF has been elucidated. Possible roles of newly identified substances, such as endothelin and EDRF, deserve investigation.

Topics: Animals; Atrial Natriuretic Factor; Dogs; Dopamine; Endothelins; Heart Failure; Kidney; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Nitric Oxide; Prostaglandins; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Vasopressins; Water-Electrolyte Imbalance

Topics: Animals; Atrial Natriuretic Factor; Heart Failure; Humans; Kidney Tubules; Neurotransmitter Agents; Prostaglandins; Renin-Angiotensin System; Signal Transduction; Vasopressins; Water-Electrolyte Imbalance

The heart functions as an endocrine organ, releasing atrial natriuretic peptide (ANP), a hormone, in response to sodium and fluid overload. Specifically, ANP is released by cardiac myocytes in response to atrial distension. As a hormone, ANP has far-reaching multiorgan effects. The body systems affected include the cardiovascular, renal, neural, gastrointestinal, and endocrine systems. However, the main effects of this hormone are on the renin-angiotensin-aldosterone system. ANP acts to oppose this system by causing vasorelaxation, blocking the secretion and sodium-retaining effects of aldosterone, and inhibiting renal renin secretion. ANP has many potential implications for clinical practice in both short-term and long-term care of patients with fluid and electrolyte balance. Clinicians may use methods to enhance or block endogenous ANP secretion based on assessment of clinical disorder, cause, status of homeostatic mechanisms, and implications for treatment. In addition, ANP may soon be administered pharmacologically, as well as monitored hematologically, in patients with fluid volume overload. In this article we describe the physiologic effects of ANP and address specific implications for clinical practice.

Topics: Animals; Atrial Natriuretic Factor; Humans; Kidney Diseases; Nursing Diagnosis; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Humans; Hyperaldosteronism; Hypertension; Natriuresis; Sodium, Dietary; Vasopressins; Water-Electrolyte Imbalance

The non-osmotic stimulation of release of arginine vasopressin (AVP) seems to be the main determinant of the impaired water excretion and hyponatraemia in patients with cardiac failure. This non-osmotic stimulation of AVP release could be secondary to a decrease in stroke volume to which the ventricular receptors respond by decreasing the vagal afferent input to the hypothalamus via the mid-brain. Improvement of cardiac stroke volume would then decrease AVP release and improve water excretion. In cardiac failure, the non-osmotic stimulation of AVP release is not clearly modulated by the renin-angiotensin system or by the atrial natriuretic peptide plasma concentration. Nevertheless, physiological concentrations of atrial natriuretic peptide could inhibit the renal epithelial water transport at the collecting duct level. Water-loading and osmotic-loading experiments in patients with cardiac failure indicated that the release of AVP is still under osmotic control and favoured the concept that volume depletion in general and cardiac failure in particular may lower the osmotic threshold and increase the osmotic sensitivity to vasopressin release. Experiments using a specific vasopressin antagonist rarely indicated a vasoconstrictor role for endogenous AVP in either experimental or clinical cardiac failure. Intrarenal factors also contributed to the impaired water excretion observed in patients with cardiac failure: increased central sympathetic efferent discharge and stimulation of the renin-angiotensin-aldosterone system would be expected as a consequence of the decreased effective arterial blood volume. These effects could then decrease maximal reabsorption of solute further impairing the ability of the kidney to excrete free water. The impaired water excretion is correlated with the severity of the cardiac deterioration and thus has prognostic implications.

Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Heart Diseases; Humans; Hyponatremia; Kidney; Prognosis; Water-Electrolyte Imbalance

Thiazolidinediones cause sodium retention and edema by a direct effect on the kidneys. The aim of this study was to use the technique of head-out water immersion to investigate the effects of rosiglitazone on sodium and volume homeostasis in subjects with type 2 diabetes mellitus. The volume expansion response to water immersion was compared with the response on a non-immersion control day in 12 nondiabetic male subjects and 8 diet-controlled male type 2 diabetic subjects with hourly blood and urine sampling over a 4-h period. This was repeated after both groups had taken 4 mg of rosiglitazone daily for 7 days. Immersion produced a natriuresis in both groups (P < 0.001). An impairment of this natriuresis was seen in the diabetic subjects (P = 0.006). However, when rosiglitazone was taken, there was no significant difference in immersion-induced natriuresis compared with nondiabetic controls (P = 0.2). There was an immersion-induced rise in atrial natriuretic peptide (ANP) and urinary cyclic guanosine monophosphate (cGMP), in the healthy subjects (ANP P = 0.001, cGMP P = 0.043), which was not seen in the diabetic subjects (ANP P = 0.51, cGMP P = 0.74). Rosiglitazone restored the immersion-induced increase in cGMP excretion and rise of ANP in the diabetic group (ANP P = 0.048, cGMP P = 0.009). This study confirms that type 2 diabetic subjects have an impaired natriuretic response to acute volume expansion, which appears to be enhanced rather than diminished by rosiglitazone. This may be related to its effects in increasing natriuretic peptides and restoring the impaired cGMP excretion to volume expansion.

Topics: Aldosterone; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Diabetes Mellitus, Type 2; Homeostasis; Humans; Hypoglycemic Agents; Immersion; Kidney; Male; Middle Aged; Natriuresis; Renin; Rosiglitazone; Thiazolidinediones; Water-Electrolyte Imbalance

Acute volume overload (AVO) induces early ischemia-like changes in intramyocardial arteries. We investigated whether the Factor Xa (FXa) inhibitor apixaban interacts with the myocardium early after AVO.. Fifty-five syngeneic Fisher rats underwent surgical abdominal aortocaval fistula to induce AVO. Among them, 17 rats were treated with apixaban (10 mg/kg/day). The myocardial outcome was studied using histological analysis and by measuring atrial natriuretic peptide (ANP) and matrix metalloprotease 9 (MMP9) gene expression.. After 3 days, the total number of intramyocardial arteries was significantly increased in the. Apixaban interacts with intramyocardial arteries in the left and right ventricles after AVO and ANP and MMP9 expression levels increased. Thus, the myocardial effect of Factor Xa inhibition needs to be monitored after AVO.

Topics: Animals; Atrial Natriuretic Factor; Factor Xa; Heart Failure; Matrix Metalloproteinase 9; Myocardium; Rats; Water-Electrolyte Imbalance

Bioimpedance spectroscopy (BIS) is widely used to assess fluid status in hemodialysis (HD) patients. Our purpose is to evaluate filtration coefficients (Lpst) as an alternative test to assess fluid status by utilizing BIS as a reference test.
. 106 HD patients (determined group) were divided into two groups with (EX group: 53) or without excess fluid mass (ExF). ExF calculated from extracellular water and intracellular water measured by BIS. Multiple linear regression equation of Lpst was made using ExF (ExF/DW) and ultrafiltration rate (UFR/DW) to adjust Lpst (AdjLpst). The cut-off values of the tests for detection of EX were determined by receiver-operator characteristic curve analysis. Lpst, AdjLpst, serum atrial natriuretic peptide concentration (ANP), ultrasonically measured inferior vena cava diameter (IVCe/BSA), and blood volume change (Δ BV/TUF/DW) were examined. The detection abilities of these tests were evaluated in the distinct 61 patients (evaluated group).
. Patients of the EX group numbered 29 in the evaluated group. The correlation between AdjLpst and ExF/DW was the highest. The sensitivity of AdjLpst and specificity of Lpst were the highest. The specificity of AdjLpst was equivalent to that of Lpst. Unadjusted and adjusted odds ratios of AdjLpst were the higher (20.80, 95% CI, 5.61-77.10, 16.06, 95% CI 4.00-64.59, respectively) than those of the other tests.
. AdjLpst can detect patients of the EX group more accurately than other tests. Because AdjLpst is related to plasma refilling, it may indicate removable fluid overload. AdjLpst in conjunction with BIS may contribute to more adequate fluid management.

Topics: Aged; Aged, 80 and over; Atrial Natriuretic Factor; Biomarkers; Blood Volume; Capillary Permeability; Electric Impedance; Fluid Therapy; Humans; Kidney Diseases; Linear Models; Logistic Models; Microvessels; Middle Aged; Multivariate Analysis; Odds Ratio; Predictive Value of Tests; Renal Dialysis; ROC Curve; Spectrum Analysis; Ultrasonography; Vena Cava, Inferior; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Increased extracellular fluid volume (ECF) characterizes compensated cirrhosis. To identify the mechanisms of fluid retention in cirrhosis through clearance methods, 10 control and 10 preascitic rats with CCl(4)-induced cirrhosis were studied following i.v. loading with 1 ml 5% glucose solution. Glomerular filtration rate and renal plasma flow were evaluated through inulin and para-aminohippurate clearances; water and electrolyte handling was assessed measuring urine and plasma osmolarity, electrolyte excretions, and tubular solute-free water reabsorption (TFWR = osmolar clearance minus urinary output); ECF was assessed through hormonal status determination. After water loading, cirrhotic rats had increased ECF (lower plasma renin activity and aldosterone and higher atrial natriuretic peptide levels, all P<0.03), solute-free water retention (increased TFWR and decreased plasma osmolarity, all P<0.05), reduced absolute and fractional sodium excretions (P<0.05). Cirrhotic rats showed sodium retention in the medullary thick ascending limb of Henle's loop (i.e. increased values of TFWR for any given value of osmolar clearance). Trans-tubular potassium gradient in medullary collecting duct was similar in the two groups (P=0.55), ruling out aldosterone-dependent sodium retention and potassium hyper-secretion. In experimental preascitic cirrhosis NaCl retention in the ascending limb of Henle's loop increases medullary interstitial tonicity leading to vasopressin-independent water back-diffusion in thin descending limb of Henle's loop and collecting duct.

Topics: Aldosterone; Animals; Atrial Natriuretic Factor; Extracellular Fluid; Glomerular Filtration Rate; Kidney; Kidney Tubules, Distal; Liver Cirrhosis; Loop of Henle; Male; Osmolar Concentration; Potassium; Rats; Rats, Wistar; Renin; Sodium; Vasopressins; Water; Water-Electrolyte Imbalance

It is well documented in literature that a majority of small-cell lung cancers are associated with paraneoplastic phenomena. We report the case of a 63-year-old man diagnosed with small-cell lung carcinoma, in whom a severe hyponatremia and renal sodium loss with inappropriate antidiuresis were also found during a routine laboratory testing. Syndrome of inappropriate antidiuretic hormone secretion was first suspected in this patient, but another complex pathogenetic mechanism involving atrial natriuretic peptides could be associated, potentiating the deflation of the plasma sodium level. In our patient, the plasma-atrial natriuretic peptide base level, determined with a sensitive radioimmunoassay, was above the normal range (183 pg/mL; normal range, 50 pg/mL, +/- 10 pg/mL), and the antidiuretic hormone plasma level had an oscillatory pattern, varying between 5.5 pg/mL and 7 pg/mL (normal range, 0-4.7 pg/mL). We discuss the pathogenesis and clinical aspects of this association and the therapeutic options for these types of patients.

Topics: Arginine Vasopressin; Atrial Natriuretic Factor; Carcinoma, Small Cell; Humans; Hyponatremia; Inappropriate ADH Syndrome; Lung Neoplasms; Male; Middle Aged; Osmolar Concentration; Paraneoplastic Syndromes; Radiography; Radioimmunoassay; Sodium; Water-Electrolyte Imbalance

To estimate the separate and combined effects of reduced P(B) and O2 levels on body fluid balance and regulating hormones, measurements were made during reduced PB (altitude, ALT; P(B) = 432 mm Hg, F(I(O2)) = 0.207), reduced inspired O2 concentration (normobaric hypoxia, HYX; P(B) = 614 mm Hg, F(I(O2)) = 0.142), and lowered ambient pressure without hypoxia (normoxic hypobaria HYB; P(B) = 434 mm Hg, F(I(O2)) = 0.296). Nine fit and healthy young men were exposed to these conditions for 10 h in a decompression chamber. Lake Louise AMS scores, urine collections, and blood samples were obtained every 3 h, with recovery measurements 2 h after exposure. AMS was significantly greater during ALT than HYX, as previously reported (J. Appl. Physiol. 81:1908-1910. 1996), because the combination of reduced P(B) and P(O2) over the 10 h favored fluid retention by reducing urine volume, while plasma volume (PV) remained higher than during HYX. At ALT the plasma Na+ fell significantly at 6 h, probably from dilution of extracellular fluid, and antidiuretic hormone (ADH) was highest (p = 0.006 versus HYB). The PV, urine flow, free water clearance, and plasma renin activity (PRA) rose significantly during recovery from ALT as AMS symptoms subsided, suggesting increased intravascular fluid and reduced adrenergic tone. During HYB, the plasma aldosterone (ALDO) and K+ levels were significantly elevated, and PRA was highest and ADH lowest, without fluid retention. During HYX, fluid balance was similar to HYB, but PV and ALDO were significantly lower, and ALDO increased significantly in recovery from HYX. The fluid retention at ALT in AMS-susceptible subjects appears related to a synergistic interaction involving reduced P(B) and ADH and ALDO.

Topics: Acclimatization; Acute Disease; Adult; Aldosterone; Altitude; Altitude Sickness; Analysis of Variance; Arginine Vasopressin; Atrial Natriuretic Factor; Body Fluids; Humans; Male; New Mexico; Norepinephrine; Renin; Water-Electrolyte Balance; Water-Electrolyte Imbalance

To examine whether children with univentricular defects have intrinsic dysfunction in the natriuretic peptide system.. We compared plasma levels of the fluid-regulating hormone vasopressin (antidiuretic hormone), aldosterone, atrial natriuretic peptide, and brain natriuretic peptide in children with congenital univentricular and biventricular defects. We enrolled 27 patients with univentricular defects and 27 patients with biventricular cardiac defects. Children who underwent Fontan and Glenn procedures were considered as patients with univentricular cardiac defects; children who underwent repair of tetralogy of Fallot or subaortic stenosis were considered as controls with biventricular defects.. Preoperative plasma atrial natriuretic peptide, brain natriuretic peptide, antidiuretic hormone, and aldosterone were comparable in both groups. Although plasma cyclic guanosine monophosphate levels were comparable between groups, there was a significant correlation between molar concentrations of plasma cyclic guanosine monophosphate and plasma atrial natriuretic peptide ( r = 0.42) and brain natriuretic peptide ( r = 0.44) in the biventricular group, but not in the univentricular group ( r = 0.19 for atrial natriuretic peptide; r = 0.13 for brain natriuretic peptide). All patients had a significant postoperative increase in plasma antidiuretic hormone. A significant postoperative increase in plasma brain natriuretic peptide was found in the patients with biventricular, but not univentricular, defects. In contrast, a significant increase in plasma aldosterone was observed only in the patients with univentricular defects.. There were distinct differences between univentricular and biventricular groups in their perioperative plasma fluid-regulating hormone responses. Specifically, patients with univentricular defects may have abnormal natriuretic peptide secretion and function. The natriuretic dysfunction may be on the basis of hypoplastic ventricular development.

Topics: Age Factors; Aldosterone; Analysis of Variance; Atrial Natriuretic Factor; Biomarkers; Cardiopulmonary Bypass; Case-Control Studies; Child, Preschool; Cyclic GMP; Down-Regulation; Female; Fontan Procedure; Heart Ventricles; Humans; Infant; Male; Mineralocorticoid Receptor Antagonists; Natriuretic Peptide, Brain; Risk Factors; Second Messenger Systems; Signal Transduction; Time Factors; Up-Regulation; Vasopressins; Water-Electrolyte Imbalance

The aim was to evaluate the factors determining preoperative renal dysfunction in patients with obstructive jaundice.. In a prospective cross-sectional observational study, 63 patients, 27 with benign and 36 with malignant obstructive jaundice, were investigated at admission and compared with 25 healthy control subjects. Variables analysed included extracellular body water (ECW) compartment, plasma levels of aldosterone, renin, atrial natriuretic peptide, vasopressin, nitric oxide, endothelin (ET) 1 and prostaglandin E2 (PGE2), urinary nitric oxide and PGE2, serum albumin and renal function.. The metabolic profile of obstructive jaundice was characterized by a depletion of the ECW (P = 0.004), and increased plasma levels of atrial natriuretic peptide (P < 0.001), ET-1 (P = 0.044), vasopressin (P = 0.017), aldosterone (P = 0.005) and renin (P = 0.001). Increased plasma (P < 0.001) and urinary (P = 0.001) PGE2 levels were also found. Fifty-four per cent of patients had a creatinine clearance of less than 70 ml/min. In multivariate analysis, serum bilirubin, renin, ET-1, PGE2, decreased urinary sodium excretion and age were identified as predictors of renal dysfunction.. Renal dysfunction in patients with obstructive jaundice was associated with the degree of biliary obstruction, age of the patient and reduced urinary sodium excretion. These alterations were closely related to derangements in sodium- and water-regulating hormones.

Topics: Atrial Natriuretic Factor; Dinoprostone; Endothelin-1; Female; Humans; Jaundice, Obstructive; Kidney Diseases; Male; Middle Aged; Multivariate Analysis; Prospective Studies; Regression Analysis; Risk Factors; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Heart Failure; Homeostasis; Humans; Myocardium; Natriuretic Peptide, Brain; Nerve Tissue Proteins; Peptide Fragments; Protein Precursors; Water-Electrolyte Imbalance

Heart failure is a leading cause of morbidity and mortality. In the United States, there are more than 5 million patients with heart failure and over 500,000 newly diagnosed cases each year. Numerous advances have been made in our understanding of the pathophysiologic mechanisms contributing to sodium and water retention in this condition. Important alterations in the sympathetic nervous system and the renin-angiotensin-aldosterone system have been described in heart failure, allowing the use of mechanism-specific treatments such as beta-adrenergic receptor antagonism and angiotensin-converting enzyme inhibition. As our understanding of the roles of the natriuretic peptides and the arginine vasopressin-aquaporin-2 system in the pathophysiology of heart failure evolves, treatments directed toward the alterations in these systems in heart failure can be further developed.

Topics: Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Atrial Natriuretic Factor; Body Fluids; Heart Failure; Humans; Natriuretic Peptide, Brain; Neurosecretory Systems; Renin-Angiotensin System; Sodium; Sympathetic Nervous System; Vasopressins; Water Intoxication; Water-Electrolyte Imbalance

Atrial natriuretic peptide (ANP) plays a part in the regulation of volume homeostasis and possibly, in the pathophysiology of water and electrolyte disorder. Patients with serious burn injuries risk huge body fluids losses, which are compensated for by perfusion. Blood volume and the renin and aldosterone system are also disturbed. This study measured plasma ANP and vasoactive intestinal polypeptide (VIP) in patients with >20% total burned surface area (TBSA), at admission and 24 h post-admission.Eleven patients (mean age 46.5 years, 8 males) with a mean TBSA of 34.5% were sampled. Standard treatment was given. Eleven closely age-matched volunteers were used as controls. A specific ELISA method suitable for the measurement of ANP and VIP was used.ANP was higher (p<0.0001), while VIP was lower (p=NS) in patients' samples compared to controls. While the level of VIP was higher at 24 h post-admission, mean ANP level remained about the same. The increased levels of plasma ANP may result from volaemic disturbances during resuscitation, low VIP levels, the increase in pulmonary resistance or post-burn stress.

Topics: Adult; Aged; Atrial Natriuretic Factor; Blood Volume; Body Surface Area; Burns; Case-Control Studies; Dehydration; Enzyme-Linked Immunosorbent Assay; Female; Fluid Therapy; Follow-Up Studies; Homeostasis; Humans; Lung; Male; Middle Aged; Patient Admission; Regional Blood Flow; Renin-Angiotensin System; Resuscitation; Skin; Statistics, Nonparametric; Vascular Resistance; Vasoactive Intestinal Peptide; Water-Electrolyte Imbalance

The Cox maze procedure has been confirmed to be effective in curing atrial fibrillation. Some authors have reported severe fluid retention after the Cox maze procedure and have suggested decreased secretion of atrial natriuretic peptide as a possible mechanism. This study was designed (1) to examine the serial changes in atrial natriuretic peptide after the Cox maze procedure as compared with changes occurring after coronary artery bypass grafting and (2) to elucidate any differences in atrial natriuretic peptide levels between patients with transient recurrence of atrial fibrillation after the Cox maze procedure and those without recurrence of atrial fibrillation.. Blood samples were drawn from the right and left atria in patients undergoing the Cox maze procedure (n = 19) and from the right atrium in patients undergoing coronary artery bypass grafting (n = 6) before and 1, 2, and 3 days after the operation. In six patients undergoing the Cox maze procedure, samples were also drawn from the radial artery before and 1, 2, 3, 5, and 7 days after the operation. The plasma samples were prepared by refrigerated centrifugation and stored until radioimmunoassay. In the Cox maze procedure group, atrial natriuretic peptide levels in the right atrium were 629 +/- 366, 154 +/- 112, 162 +/- 112, and 183 +/- 97 pg/ml and those in the left atrium were 276 +/- 168, 152 +/- 91, 162 +/- 111, and 145 +/- 80 pg/ml before and 1, 2, and 3 days after the operation, respectively. A marked decrease in atrial natriuretic peptide levels was evident after the Cox maze procedure (p < 0.001). There was no significant correlation between atrial natriuretic peptide levels and atrial pressures after the Cox maze procedure, which suggests that secretion of atrial natriuretic peptide by the atria was impaired. There was a significant correlation between the atrial natriuretic peptide levels in the left atrium and those in the peripheral radial artery, and the decreased levels of atrial natriuretic peptide in the radial artery continued for 7 days after the Cox maze procedure. There were no differences in the atrial natriuretic peptide levels between the patients with transient recurrence of atrial fibrillation (n = 6) and those without recurrence (n = 13) after the Cox maze procedure. In the coronary artery bypass grafting group, the atrial natriuretic peptide levels in the right atrium were 115 +/- 37, 124 +/- 48, 154 +/- 54, and 156 +/- 36 pg/ml before and 1, 2, and 3 days after the operation, respectively. No change was seen after the operation.. We observed a significant decrease in atrial natriuretic peptide levels after the Cox maze procedure. This may be one of the possible causes of fluid retention after this procedure. These decreased atrial natriuretic peptide levels after the Cox maze procedure may result from the multiple atriotomy incisions and excision of both atrial auricles performed during the procedure, rather than from the conversion of atrial fibrillation to normal sinus rhythm.

Topics: Atrial Fibrillation; Atrial Function; Atrial Natriuretic Factor; Cardiac Surgical Procedures; Case-Control Studies; Coronary Artery Bypass; Female; Humans; Male; Middle Aged; Postoperative Complications; Radial Artery; Recurrence; Water-Electrolyte Imbalance

Chronic schizophrenic patients are reported to develop imbalanced water homeostasis by the pathological secretion of vasopressin and aldosterone. We measured plasma vasopressin, aldosterone and atrial natriuretic peptide in schizophrenic patients to elucidate the role of these hormones during a perioperative period. Eighteen schizophrenic patients with chronic antipsychotic drugs over 10 years and 22 as a control group who underwent elective lower abdominal surgery were the subjects of this study. In the schizophrenic patients, plasma aldosterone secretion was significantly inhibited, while plasma vasopressin and atrial natriuretic peptide were significantly increased during surgery. A good relationship (r = 0.69, p < 0.01) between plasma atrial natriuretic peptide and plasma osmolality was obtained 60 min after skin incision, but not before the induction of anesthesia. The findings suggest that chronic schizophrenic patients may develop an abnormal secretion of vasopressin, aldosterone and atrial natriuretic peptide during anesthesia.

Topics: Adult; Aged; Aldosterone; Atrial Natriuretic Factor; Case-Control Studies; Chronic Disease; Dopamine; Female; Humans; Intraoperative Period; Linear Models; Male; Middle Aged; Osmolar Concentration; Prospective Studies; Schizophrenia; Time Factors; Vasopressins; Water-Electrolyte Imbalance

Hyponatremia after pituitary surgery is presumed to be due to antidiuresis; however, detailed prospective investigations of water balance that would define its pathophysiology and true incidence have not been established. In this prospective study, the authors documented water balance in patients for 10 days after surgery, monitored any sodium dysregulation, further characterized the pathophysiology of hyponatremia, and correlated the degree of intraoperative stalk and posterior pituitary damage with water balance dysfunction. Ninety-two patients who underwent transsphenoidal pituitary surgery were studied. To evaluate posterior pituitary damage, a questionnaire was completed immediately after surgery in 61 patients. To examine the osmotic regulation of vasopressin secretion in normonatremic patients, water loads were administered 7 days after surgery. Patients were categorized on the basis of postoperative plasma sodium patterns. After pituitary surgery, 25% of the patients developed spontaneous isolated hyponatremia (Day 7 +/- 0.4). Twenty percent of the patients developed diabetes insipidus and 46% remained normonatremic. Plasma arginine vasopressin (AVP) was not suppressed in hyponatremic patients during hypoosmolality or in two-thirds of the normonatremic patients after water-load testing. Only one-third of the normonatremic patients excreted the water load and suppressed AVP normally. Hyponatremic patients were more natriuretic, had lower dietary sodium intake, and had similar fluid intake and cortisol and atrial natriuretic peptide (ANP) levels compared with normonatremic patients. Normnonatremia, hyponatremia, and diabetes insipidus were associated with increasing degrees of surgical manipulation of the posterior lobe and pituitary stalk during surgery. The pathophysiology of hyponatremia after transsphenoidal surgery is complex. It is initiated by pituitary damage that produces AVP secretion and dysfunctional osmoregulation in most surgically treated patients. Additional events that act together to promote the clinical expression of hyponatremia include nonatrial natriuretic peptide-related excess natriuresis, inappropriately normal fluid intake and thirst, as well as low dietary sodium intake. Patients should be monitored closely for plasma sodium, plentiful dietary sodium replacement, mild fluid restriction, and attention to symptoms of hyponatremia during the first 2 weeks after transsphenoidal surgery.

Topics: Adult; Arginine Vasopressin; Atrial Natriuretic Factor; Child; Diabetes Insipidus; Diuresis; Female; Fluid Therapy; Humans; Hydrocortisone; Hyponatremia; Incidence; Intraoperative Complications; Male; Natriuresis; Pituitary Diseases; Pituitary Gland; Pituitary Gland, Posterior; Postoperative Complications; Prospective Studies; Renal Agents; Sodium; Sodium, Dietary; Sphenoid Bone; Thirst; Vasopressins; Water; Water-Electrolyte Balance; Water-Electrolyte Imbalance

A state of normokalemic renal sodium wasting associated with an apparently inappropriate secretion of atrial natriuretic peptide (ANP) has not been previously recognized. We here report an 11-year-old boy who presented with a chronic "salt-losing" nephropathy manifested by normonatremic or mildly hyponatremic extracellular fluid volume depletion, hypodipsia, absence of salt appetite, normokalemic metabolic alkalosis, hyper-reninemic hyperaldosteronism, hypertrophy of the juxtaglomerular apparatus, and highly conserved capacities for concentrating diluting the urine. Plasma ANP values were paradoxically elevated (between 10 and 47 fmol/ml), despite the coexistence of intravascular volume depletion and increased plasma levels of renin and aldosterone. Although the patient had some clinical similarities to Bartter's syndrome, fractional sodium chloride (NaCl) reabsorption during hypotonic saline diuresis was normal and no clinical amelioration was observed while on indomethacin therapy. Neither a tumor nor cardiac or cerebral abnormalities, which could be responsible for the increased ANP secretion, were detected. These clinical, biochemical, and histological features have not been previously described together and may represent a new clinical syndrome. The pathophysiology of this entity remains unknown, but an attractive, although unproven, hypothesis is that the renal defect in NaCl reabsorption in this patient could be related to an inappropriate and unregulated secretion of ANP.

Topics: Aldosterone; Atrial Natriuretic Factor; Blood Volume; Child; Cyclooxygenase Inhibitors; Electrocardiography; Humans; Indomethacin; Kidney; Kidney Diseases; Male; Sodium; Sodium, Dietary; Syndrome; Water-Electrolyte Imbalance

This study was designed to investigate disturbances in arterial blood pressure and body fluid homeostasis in stable heart transplant recipients.. Hypertension and fluid retention frequently complicate heart transplantation.. Blood pressure, renal and endocrine responses to acute volume expansion were compared in 10 heart transplant recipients (57 +/- 9 years old [mean +/- SD]) 20 +/- 5 months after transplantation, 6 liver transplant recipients receiving similar doses of cyclosporine (cyclosporine control group) and 7 normal volunteers (normal control subjects). After 3 days of a constant diet containing 87 mEq/24 h of sodium, 0.154 mol/liter saline was infused at 8 ml/kg per h for 4 h. Blood pressure and plasma vasopressin, angiotensin II, aldosterone, atrial natiuretic peptide and renin activity levels were determined before and at 30, 60, 120 and 240 min during the infusion. Urine was collected at 2 and 4 h. Blood pressure, fluid balance hormones and renal function were monitored for 48 h after the infusion.. Blood pressure did not change in the two control groups but increased in the heart transplant recipients (+15 +/- 8/8 +/- 5 mm Hg) and remained elevated for 48 h (p < or = 0.05). Urine flow and urinary sodium excretion increased abruptly in the control groups sufficient to account for elimination of 86 +/- 9% of the sodium load by 48 h; the increases were blunted (p < or = 0.05) and delayed in the heart transplant recipients, resulting in elimination of only 51 +/- 13% of the sodium load. Saline infusion suppressed vasopressin, renin activity, angiotensin II and aldosterone in the two control groups (p < or = 0.05) but not in the heart transplant recipients. Heart transplant recipients had elevated atrial natriuretic peptide levels at baseline (p < or = 0.05), but relative increases during the infusion were similar to those in both control groups.. Blood pressure in heart transplant recipients is salt sensitive. These patients have a blunted diuretic and natriuretic response to volume expansion that may be mediated by a failure to reflexly suppress fluid regulatory hormones. These defects in blood pressure and fluid homeostasis were not seen in liver transplant recipients receiving cyclosporine and therefore cannot be attributed to cyclosporine alone. Abnormal cardiorenal neuroendocrine reflexes, secondary to cardiac denervation, may contribute to salt-sensitive hypertension and fluid retention in heart transplant recipients.

Topics: Angiotensin II; Arginine Vasopressin; Atrial Natriuretic Factor; Blood Pressure; Case-Control Studies; Cyclosporine; Female; Heart; Heart Transplantation; Humans; Hypertension; Immunosuppressive Agents; Liver Transplantation; Male; Middle Aged; Renin-Angiotensin System; Sodium Chloride; Sodium, Dietary; Ventricular Function, Left; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Plasma concentrations of atrial natriuretic peptide (ANP) and its second messenger cyclic guanosine-monophosphate (cGMP) were studied in 28 children and adolescents (1 to 19 years) on peritoneal dialysis and compared to 55 healthy children (1 to 20 years). Dialysate concentrations of the hormones were measured also in the patients. Plasma ANP was not significantly different in patients and controls (28.8 pmol/l [15.5-53.6 pmol/l] [median, lower and upper quartile] versus 26.3 pmol/l [19.9-31.8 pmol/l]). In seven children on peritoneal dialysis it exceeded an upper normal limit of 50 pmol/l, but it fell to normal values in four of them after forced fluid withdrawal. Plasma cGMP was elevated in the patients compared to the control children (1.6 nmol/l [1.1-1.7 nmol/l] versus 1.0 nmol/l [0.8-1.2 nmol/l]; p < 0.05). There were only weak correlations between plasma and dialysate concentrations of ANP and cGMP. Plasma concentrations of ANP seem to be elevated in children on peritoneal dialysis in case of fluid overload.

Topics: Adolescent; Atrial Natriuretic Factor; Child; Cyclic GMP; Female; Humans; Kidney Failure, Chronic; Male; Peritoneal Dialysis; Peritoneal Dialysis, Continuous Ambulatory; Radioimmunoassay; Reference Values; Water-Electrolyte Imbalance

The common disorders of fluid, electrolyte and acid-base metabolism observed in patients with liver cirrhosis are hyponatremia, hypokalemia, respiratory alkalosis, and metabolic acidosis, in addition to an excess accumulation of body fluids with edema and ascites formation. It has been suggested that an impaired renal sodium excretion in liver cirrhosis is caused by rather an increase in tubular sodium reabsorption than a decrease in glomerular filtration rate. In order to explain the pathophysiological mechanisms involved in initiating and maintaining sodium retention in cirrhosis, three hypotheses, namely, the "underfilling" hypothesis, the "overflow" hypothesis, and the "pepipheral arterial vasodilation" hypothesis have been proposed. However, neither of them could not fully account for the pathogenesis and pathophysiology of the avid renal sodium retention in cirrhosis. Although it is undoubted that the abnormal renal sodium handling in cirrhosis is mediated mainly by the sympathetic nervous system and the certain humoral agents such as renin-angiotensin-aldosterone system, atrial natriuretic peptide, prostaglandins, kallikein-kinin system, antidiuretic hormone and so on, the precise mechanism of the enhanced tubular sodium reapsorption induced via these factors is not well understood and still remains to be elucidated.

Topics: Acid-Base Imbalance; Atrial Natriuretic Factor; Humans; Kallikreins; Kinins; Liver Cirrhosis; Renin-Angiotensin System; Water-Electrolyte Imbalance

This study investigated the pathogenesis of water and sodium metabolism derangements in obstructive jaundice.. Obstructive jaundice is associated with hypodipsia, depletion of extracellular water, alterations of the water and sodium regulating hormones, and an increased incidence of renal failure. Plasma atrial natriuretic factor (ANF) increases after common bile duct ligation in the rabbit. The present study was designed to investigate ANF-secreting cardiac atrial cells in this animal model.. Plasma ANF and the percentage of atrial cells staining for ANF were determined in jaundiced and sham-operated rabbits at 24 (group OJ-24, n = 11; group SO-24, n = 5) and 72 hours (group OJ-72, n = 11; group SO-72, n = 5) after surgery. The atrial ANF content was also determined.. Plasma ANF was higher in jaundiced animals than in controls both at 24 (63 +/- 44 fmol/mL vs. 17 +/- 10 fmol/mL, p < 0.02) and at 72 hours (73 +/- 49 fmol/mL vs. 12 +/- 11 fmol/mL). In the two OJ groups, the percentage of positive ANF cells per 200-power field in the right atrial appendage was higher than in the SO groups both at 24 (62 +/- 11% vs. 31 +/- 12%, p < 0.003) and at 72 hours (56 +/- 18% vs. 31 +/- 12%, p < 0.01). Similar results were obtained in the right auricular wall. The percentage of positive ANF cells was significantly higher in the left atrium in which significant differences between the OJ and SO groups were also noted. The right atrial ANF content was higher in the OJ than in SO groups (437 +/- 323 pmol/mg of protein vs. 83 +/- 44 pmol/mg of protein).. Cardiac endocrine activity is increased in experimental obstructive jaundice. ANF may be involved in the pathogenesis of the renal and water and sodium metabolic disturbances present in this disease.

Topics: Animals; Atrial Natriuretic Factor; Cholestasis; Common Bile Duct; Common Bile Duct Diseases; Heart Atria; Ligation; Rabbits; Renal Insufficiency; Water-Electrolyte Imbalance

Topics: Adult; Atrial Natriuretic Factor; Biomarkers; Cyclic GMP; Female; Humans; Male; Middle Aged; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis; Water-Electrolyte Imbalance

To investigate the mechanism of water and sodium retention during PEEP ventilation, ten dogs were studied at 0, 1.33Kpa, 2.67Kpa PEEP and at spontaneous breathing. Hemodynamics, renal excretory function parameters and plasma hormonal parameters were recorded at the end of each period. Compared with spontaneous breathing, PEEP induced a significant reduction of diuresis (from 31.8 +/- 17.9 to 11.2 +/- 6.4ml/h, P < 0.01) and natriuresis (from 5.21 +/- 4.93 to 1.09 +/- 1.22 mmol/h, P < 0.01), whereas plasma atrial natriuresis factor (ANF) fell from 1219 +/- 446 to 713 +/- 344 pg/ml (P < 0.05) and esophageal pressure increased from 0.13 +/- 0.42 to 1.22 +/- 0.66Kpa (P < 0.01), serum aldosterone (ALD) increased from 295 +/- 281 to 1012 +/- 685 pg/ml (P < 0.05). There was a significant correlation between ANF and ALD (r = -0.647, P < 0.001). We suggest that changes in ANF in response to intrathoracic pressure may contribute to alteration of renal excretory function during PEEP.

Topics: Aldosterone; Animals; Atrial Natriuretic Factor; Diuresis; Dogs; Female; Male; Natriuresis; Positive-Pressure Respiration; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Humans; Liver Cirrhosis; Natriuresis; Renin-Angiotensin System; Water-Electrolyte Imbalance

Plasma atrial natriuretic peptide (ANP) and cyclic 3'5'-guanosine monophosphate (cGMP) were investigated as indicators of fluid volume overload in children and adolescents with chronic renal failure. Plasma ANP and cGMP were measured in both paediatric patients with chronic renal failure (n = 17, mean serum creatinine 371 +/- 242 mumol/l) and those with end-stage renal disease on haemodialysis (n = 18). cGMP was higher in children with chronic renal failure than in 45 healthy controls (1.0 +/- 0.4 vs 2.1 +/- 0.8 nmol/l, P less than 0.01), whereas plasma ANP was similar (26.9 +/- 9.7 vs 34.0 +/- 12.3 pmol/l). Both ANP and cGMP were markedly elevated in children with end-stage renal disease before haemodialysis and fell significantly during dialysis. During dialysis body weight decreased by 1.6 +/- 0.7 kg, corresponding to 4.5 +/- 2.1% of body weight. Plasma ANP correlated positively with plasma cGMP in haemodialysed patients (r = 0.43, P less than 0.05). Reduction in body weight and in mean arterial pressure correlated more closely with plasma ANP than with cGMP. Therefore, elevation of plasma ANP appears to indicate volume overload in children undergoing haemodialysis, but whether it can be used also in children with chronic renal failure requires further investigation.

Topics: Adolescent; Adult; Atrial Natriuretic Factor; Blood Volume; Body Weight; Child; Child, Preschool; Creatinine; Cyclic GMP; Female; Humans; Kidney Failure, Chronic; Male; Renal Dialysis; Water-Electrolyte Imbalance

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

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

Topics: Adult; Alcohol Withdrawal Delirium; Alcoholism; Aldosterone; Atrial Natriuretic Factor; Central Nervous System; Humans; Male; Radioimmunoassay; Renin; Sodium; Water-Electrolyte Imbalance

Previous studies have shown that common bile duct ligation in the rabbit is followed by a reduction of the extracellular water compartment. To further elucidate the mechanisms leading to volume depletion in this model, water and sodium balances and changes in plasma concentrations of atrial natriuretic peptide (ANP), vasopressin (ADH), plasma renin activity (PRA) and aldosterone (Ald) were investigated during the first 4 days after common bile duct ligation (group OJ,) or sham operation (group SO). Water and chow intakes were lower in group OJ (148 +/- 30 versus 226 +/- 40 mL/4 days; p = 0.004 and 12 +/- 9 versus 171 +/- 40 g/4 days; p = 0.0001). There were no differences in urine output. Sodium urinary losses were marginally higher in group OJ (12.4 +/- 7 versus 6.7 +/- 5 mEq/4 days; p = 0.06). Water balance was lower in group OJ (-50 +/- 56 versus 101 +/- 71 mL/4 days; p = 0.0001). At 24 hours, plasma ANP (41 +/- 7 versus 10.7 +/- 1 fmol/mL, p = 0.0001), ADH (21.8 +/- 7 versus 12.3 +/- 6 pg/mL, p = 0.008) and Ald (14.5 +/- 5 versus 3.7 +/- 3 ng/dL, p = 0.001) were higher in group OJ. These alterations persisted 72 hours after bile duct ligation, when a concomitant increase in PRA (10.7 +/- 5 versus 3 +/- 1.6 ng/dL, p = 0.006) was also observed. A group of pair-fed pair-watered sham-operated controls (group SO2, n = 13) showed a metabolic profile similar to group OJ but a low ANP concentration. Multiple venous sampling in five rabbits 24 hours after bile duct ligation showed the highest plasma levels of ANP in the aorta and infrarenal vena cava. These results suggest that common bile duct ligation in the rabbit is followed by marked hypodipsia and hypophagia, possibly mediated by ANP, leading to isotonic volume depletion and secondary activation of the water and sodium retaining hormones.

Topics: Acute Kidney Injury; Aldosterone; Animals; Atrial Natriuretic Factor; Cholestasis; Common Bile Duct; Ligation; Male; Natriuresis; Rabbits; Renin; Time Factors; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Atriopulmonary anastomosis results in a chronic right atrial pressure-volume overload. Water and salt retention is a frequent clinical observation in patients after atriopulmonary anastomosis. The purpose of this study was to examine if this could be related to an inability to increase already elevated circulating atriopeptin (ANP) in response to central volume-overloading conditions. Eighteen patients (mean age 16 +/- 6 years) with an atriopulmonary anastomosis underwent routine cardiac catheterization during which a 5-minute head-down 10 degrees tilt was performed. Peripheral venous and right atrial blood samples were obtained under basal conditions, and after tilting and angiography for determination of ANP concentrations. At a different time, circulating ANP levels were measured during a maximal graded exercise protocol. Increased circulating ANP concentrations were found under basal conditions (114 +/- 10 pg/ml). Tilting and cardioangiography resulted in significant increases in mean atrial pressure (basal: 12 +/- 0.7 mm Hg; tilt: 13.4 +/- 0.63 mm Hg; after angiography: 15.8 +/- 0.8 mm Hg), but not in atrial or peripheral ANP. Compared with the expected threefold increase in plasma ANP induced by maximal exercise in healthy control subjects, only a slight (0.25-fold) increase was found in patients. These observations suggest a reduced stimulus-release response after atriopulmonary anastomosis, which could be related to a loss of atrial stretch receptor sensitivity, achievement of the limit for maximal right atrial secretion, or an alteration in right atrial compliance, or a combination.

Topics: Adolescent; Adult; Anastomosis, Surgical; Angiocardiography; Atrial Natriuretic Factor; Child; Diuresis; Exercise Test; Female; Heart Atria; Humans; Male; Natriuresis; Postoperative Complications; Posture; Pulmonary Artery; Water-Electrolyte Imbalance

Topics: Atrial Natriuretic Factor; Cardiac Output, Low; Humans; Male; Middle Aged; Myocardium; Renal Dialysis; Water-Electrolyte Imbalance

Topics: Adaptation, Physiological; Arginine Vasopressin; Atrial Natriuretic Factor; Drinking; Extracellular Space; Humans; Hyponatremia; Water-Electrolyte Balance; Water-Electrolyte Imbalance

It is commonly taught that retention of free water is the dominant factor reducing the serum sodium concentration in hyponatremia. To determine whether the concentrations of other electrolytes are similarly diluted, we identified 51 patients with hyponatremia (Na = 121 +/- 1 mmol/L [mEq/L]) and compared electrolyte and laboratory values at the time of hyponatremia with values at a time when serum sodium was in the normal range (138 +/- 1 mmol/L). The medium interval between these measurements was 12 days. At the time of hyponatremia, serum sodium and chloride were substantially and significantly reduced by 12% to 15%. Although many hyponatremic patients had overtly increased or decreased concentrations of the other measured electrolytes, there were no significant changes in the mean concentration for any of these at the time of hyponatremia. Unchanged mean values were found for the plasma concentration of bicarbonate (26.1 +/- 0.6 normal v 25.2 +/- 0.8 mmol/L at the time of hyponatremia), potassium (4.31 +/- 0.10 v 4.33 +/- 0.15 mmol/L), albumin, phosphate, and creatinine. The stability of these laboratory values was observed both in patients with clinically normal extracellular fluid (ECF) volume and in those with true or effective ECF depletion. The urinary sodium (UNa) concentration was found to be a reliable predictor of the ECF volume status, whereas the fractional sodium excretion (FENa) was not. Electrolyte derangements are common in patients with hyponatremia, but are usually confined to patients on diuretics or who have an abnormal ECF volume. In the absence of these complicating situations, the plasma electrolytes are typically normal and are not reduced by dilution to the same extent as Na and CI. Based on a review of both the classic and recent knowledge concerning electrolyte regulation in hyponatremia, we propose that two factors explain these observations. First, the degree of dilution is overestimated because of Na losses in urine and perhaps Na shift into cells. Second, both renal and extrarenal adaptive mechanisms are activated by hyponatremia that stabilizes the concentration of other ions. One of these mechanisms is cell swelling, which triggers a volume-regulatory response leading to the release of ions and water into the ECF. Other adaptive mechanisms are mediated by antidiuretic hormone (ADH) per se, and by atrial natriuretic peptide (ANP).

Topics: Adaptation, Physiological; Animals; Atrial Natriuretic Factor; Bicarbonates; Extracellular Space; Humans; Hyponatremia; Incidence; Potassium; Retrospective Studies; Urea; Uric Acid; Vasopressins; Water-Electrolyte Balance; Water-Electrolyte Imbalance

Sodium retention in cirrhosis has been attributed to an imbalance between vasoconstrictive antinatriuretic forces such as the sympathetic nervous system and vasodilatory natriuretic agents such as atrial natriuretic factor (ANF). With the development of refractory ascites, cirrhotic patients become unresponsive to the natriuretic effect of ANF. Animal data suggest that the sympathetic nervous system plays a key role in mediating the refractoriness to ANF. We therefore studied the relationship between sympathetic nerve activity (SNA) and the natriuretic response to ANF in normal subjects and cirrhotic patients. We also attempted to localize the intrarenal site of refractoriness to ANF by lithium clearance.. Twenty-six patients with biopsy-proven cirrhosis and seven age- and sex-matched normal volunteers were studied after a week of 20 mmol/day sodium intake and no diuretics. Muscle SNA was recorded from the peroneal nerve (microneurography) and correlated with responsiveness to a 2-hour ANF infusion. Lithium clearance was used as a marker of sodium reabsorption proximal to the intramedullary collecting duct, the main site of ANF action. Plasma norepinephrine, renin, and aldosterone levels were also determined. Patients were categorized into three groups: nine patients free of ascites (by ultrasonography), five ascitic patients who responded to a 2-hour ANF infusion (i.e., had a natriuretic response to ANF above 0.83 mmol/hour), and 12 ascitic patients who did not respond.. Muscle SNA was greatly increased in the ascitic nonresponder patients compared with the normal subjects (64 +/- 4 versus 27 +/- 7 bursts/minute, p less than 0.001), moderately increased in ascitic responders (47 +/- 6 bursts/minute, p less than 0.05), but not significantly increased in nonascitic patients with cirrhosis (34 +/- 5 bursts/minute). SNA was positively correlated with plasma norepinephrine levels (r = 0.69; p less than 0.005) and inversely correlated with peak sodium excretion during the ANF infusion (r = -0.63; p less than 0.001). Plasma renin activity and aldosterone were markedly elevated in ascitic nonresponders, and normal in ascitic responders and nonascitic patients. Lithium clearance was reduced in ascitic patients compared with nonascitic patients, did not change after the ANF infusion, and correlated inversely with SNA (r = -0.61; p less than 0.01).. These results support the concept that the sympathetic nervous system is a factor in renal sodium handling in cirrhosis, especially in the initiation of sodium retention and the development of refractory ascites. Refractoriness to ANF might be explained, at least in part, by increased neurally mediated sodium reabsorption proximal to the intramedullary collecting duct, the main site of ANF action.

Topics: Adult; Aldosterone; Ascites; Atrial Natriuretic Factor; Female; Hemodynamics; Humans; Kidney Tubules, Proximal; Lithium; Liver Cirrhosis; Male; Metabolic Clearance Rate; Middle Aged; Muscles; Norepinephrine; Renin; Severity of Illness Index; Sodium; Sympathetic Nervous System; Water-Electrolyte Imbalance

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

Two peptides consisting of amino acids 1-30 and 31-67 of the N-terminus of the prohormone of atrial natriuretic factor (pro-ANF) that have vasodilatory and natriuretic properties were investigated to determine if they circulate in humans. Specific and sensitive radioimmunoassays were developed to amino acids 1-30, 31-67, and 99-126 of pro-ANF. Evaluation of human plasma that had been subjected to reverse-phase high-pressure liquid chromatography suggested that pro-ANFs 1-30 and 31-67 as well as ANF were distinct peaks in human plasma corresponding exactly to pure synthetic peaks of these peptides on high-pressure liquid chromatography. Molecular weight determination of the endogenous immunoreactive peptides measured in plasma by G-50 Sephadex gel permeation chromatography revealed that the pro-ANF 1-30 radioimmunoassay recognized a peptide of 10,000 MW, which is consistent with it measuring the whole N-terminus of pro-ANF (amino acids 1-98) but without ANF (C-terminus) attached to it. The pro-ANF 31-67 radioimmunoassay recognized mainly (more than 95%) a peptide of 3,900-4,000 MW, which corresponds closely with its actual molecular weight of 3,878. Our ANF radioimmunoassay recognizes a peptide in plasma of 3,000 MW with the known molecular weight of ANF being 3,081. The mean circulating concentrations of immunoreactive pro-ANF 1-98, pro-ANF 31-67, and ANF in 54 control subjects were 531 +/- 25, 371 +/- 18, and 22 +/- 1 fmol/ml (+/- SEM), respectively. Thirty patients with varying severity of congestive heart failure were also studied. The N-terminus, C-terminus, and pro-ANF 31-67 increased: twofold for New York Heart Association functional Class II, threefold to ninefold for Class III, and 10- to 20-fold for Class IV patients with congestive heart failure. Thus, the N-terminus and a 4,000-MW peptide from the midportion of the N-terminus of pro-ANF as well as ANF circulate normally and increased proportionately to the increasing severity of congestive heart failure. However, because the pro-ANF 31-67 radioimmunoassay was the only assay that discriminated between patients with Class I congestive heart failure and control subjects, this assay may be the most useful to accurately classify the severity of congestive heart failure.

Topics: Adult; Atrial Natriuretic Factor; Chromatography, High Pressure Liquid; Female; Heart Failure; Humans; Male; Middle Aged; Molecular Weight; Peptide Fragments; Peptide Termination Factors; Protein Precursors; Radioimmunoassay; Water-Electrolyte Imbalance

Imbalance of water and electrolytes in the elderly was investigated. In the elderly, hyponatremia is the most common electrolyte imbalance disorder and half of the cases with hyponatremia are accompanied by malignancy. It is well known that renal function decreases with ageing, and hyporeninemic hypoaldosteronism, relative AVP unresponsiveness and high level of plasma ANP are observed in the elderly. Therefore, renin-aldosterone system, AVP and ANP as well as renal function of the elderly were studied. AVP response to osmotic stimulus in the elderly increased, indicating that osmostat hypersensitivity existed in the elderly. The response of ANP to hypertonic saline infusion was well preserved. Increase in FENa with decrease in GFR and decreased salt-retaining renal capacity, with low response of the renin-aldosterone system, under low salt intake were observed in the elderly. Therefore, the low response of renin-aldosterone system may be, in part, involved in the pathophysiology. Plasma ANP positively correlated with FENa and the rate of the response of FENa to endogenous ANP was lower in the elderly than in young adults. In addition, the ANP disappearance rate from plasma in the elderly decreased. It was, therefore, suggested that those factors might be, in part, responsible for the increase in plasma ANP level. Accordingly, a high plasma ANP level might be relatively non-contributory to hyponatremia in the elderly. In summary, hyponatremia is the most common disorder of electrolyte imbalance in the elderly.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Aged; Aging; Arginine Vasopressin; Atrial Natriuretic Factor; Humans; Renin-Angiotensin System; Water-Electrolyte Imbalance

Topics: Animals; Atrial Natriuretic Factor; Cytoplasmic Granules; Endocrine Glands; Heart; Microscopy, Electron; Myocardium; Protein Precursors; Rats; Rats, Inbred Strains; Water-Electrolyte Imbalance

Circulating amounts of human atrial natriuretic peptide (hANP) are elevated in congestive heart failure and renal failure. Stretching of cardiac atria, due to volume expansion associated with these diseases, is widely accepted to be the predominant stimulus for release of the hormone. Measurements of hemodynamic parameters as well as plasma concentrations of ANP in the right cardiac atrium, pulmonary artery, radial artery and vena cava superior, before and after continuous veno-venous hemofiltration (CVVH) of critically ill volume expanded patients, proved that ANP might be a useful indicator of fluid balance in these patients.

Topics: Atrial Natriuretic Factor; Blood; Heart Failure; Humans; Kidney Failure, Chronic; Ultrafiltration; Water-Electrolyte Imbalance

There are no reliable parameters for the detection of fluid overload in anuric patients. In 70 patients on regular haemodialysis (HD) or haemofiltration (HF) treatment, plasma ANP IR concentrations were determined by radioimmunoassay and compared to 43 controls with normal renal function. ANP IR levels were markedly elevated immediately before HD or HF (m 82 fmol/ml) compared to ANP IR plasma concentrations after HD or HF (m 42 fmol/ml) and to ANP IR levels of healthy controls (m 19 fmol/ml). ANP IR was detected in haemofiltrates and found to be eliminated by HF. During isovolemic HF, ANP IR levels remained constant suggesting that ANP synthesis is much higher than elimination by HF and that the decrease in circulating volume at the end of HF or HD is the main stimulus for a lower secretion rate of ANP. Elevated ANP IR levels at the end of HD/HF were found to be associated with fluid overload even without clinical or radiographic symptoms. Consistent weight reduction was followed by a decrease of ANP IR levels.

Topics: Adolescent; Adult; Aged; Atrial Natriuretic Factor; Body Weight; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Radioimmunoassay; Renal Dialysis; Ultrafiltration; Water-Electrolyte Imbalance

Although controlled mechanical ventilation (CMV) with positive end-expiratory pressure (PEEP) has a central place in the treatment of acute respiratory failure (ARF), several side effects of this technique have to be faced. CMV with PEEP may induce pulmonary barotrauma, disturbance of cardiac performance, impairment of renal function and fluid retention. Atrial natriuretic peptides (ANP) are released from the atria upon stretching and play a major role in the control of sodium and fluid balance. Therefore it was logical to determine plasma levels of alpha-ANP in CMV. A study performed in 7 patients suffering from ARF suggested that alpha-ANP plasma levels were depressed during PEEP at 15 cm H2O in comparison with PEEP at 0 cm H2O (ZEEP). The decrease in plasma levels of alpha-ANP was evident in samples taken from superior vena cava, right atrium, pulmonary artery and radial artery as well. The decrease in alpha-ANP was associated with a decline in cardiac index, creatinine clearance, urinary output and urinary sodium excretion. Experiments in volume- expanded healthy volunteers also suggest that CMV with PEEP is able to depress plasma levels of alpha-ANP. The reasons behind the decline in release of alpha-ANP may be atrial compression by the distended lungs and the well-known reduction of venous return to the heart. Other possible factors promoting fluid retention during CMV with PEEP are the decrease in cardiac index and glomerular filtration rate, changes in intrarenal distribution of blood flow, and a stimulation of release of antidiuretic hormone via stretch receptors in the left atrium and baroreceptors in aorta and carotid arteries.

Topics: Animals; Atrial Natriuretic Factor; Humans; Kidney; Positive-Pressure Respiration; Respiratory Distress Syndrome; Vasopressins; Water-Electrolyte Imbalance

Fluid and electrolyte homeostasis is impaired in patients suffering from hypothyroidism and myxedema because myxedema induces retention of salt and water. We have measured plasma levels of human atrial natriuretic peptide (hANP) in 8 female patients who had been totally thyroidectomized because of thyroid carcinoma. Estimations of the hormone were done 4 weeks after diagnostic withdrawal (searching for iodine retaining metastases) and after 2 weeks and 4 weeks of reinitiation of thyroid suppressive therapy by L-thyroxine. hANP levels, although within the normal range (10-80 ng/l) throughout the study, were positively linked to the amount of pericardial effusion (determined by echocardiography), which was highest initially and decreased or vanished with duration of L-thyroxine therapy. Additionally, a positive correlation between thyroid hormone levels and hANP was obtained when the counteracting effect of pericardial effusion was allowed for by partial correlation analysis. Our findings might facilitate explanation of mild polyuria in hyperthyroidism and impaired water excretion in hypothyroidism.

Topics: Adult; Atrial Natriuretic Factor; Female; Humans; Middle Aged; Pericardial Effusion; Thyroid Diseases; Thyroid Hormones; Water-Electrolyte Imbalance

Responses of atrial mRNA, atrial peptide and plasma peptide of atrial natriuretic factor (ANF) to treatments to alter fluid volume were studied in rats using RNA dot hybridization assay and radioimmunoassay. Specific changes in the level of ANF mRNA relative to total atrial RNA were observed in atria from sodium restricted rats and water deprived then sodium loaded rats, demonstrating an association of change in water-sodium balance with the expression of ANF gene. The levels of mRNA and the immunoreactive ANF in plasma decreased to 30% and 15% of controls, respectively, on water-deprivation and then increased again to control levels after administering 1.8% NaCl solution, whereas atrial immunoreactive ANF increased to about twice the control on water-deprivation and decreased again after supplying NaCl solution, in parallel with the level of the hematocrit. These findings suggest that atrial ANF content is dependent more on ANF release than on biosynthesis.

Topics: Animals; Atrial Natriuretic Factor; DNA; Heart Atria; Heart Ventricles; Male; Muscle Proteins; Nucleic Acid Hybridization; Radioimmunoassay; Rats; Rats, Inbred Strains; RNA, Messenger; Sodium; Water-Electrolyte Imbalance