Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

58 patients (mean age 51 years) with cirrhosis of the liver were studied. 16 patients were compensated, 18 decompensated with ascites, and 24 decompensated and treated with diuretics. Basal plasma levels of atrial natriuretic peptide were not different between any groups of cirrhotic patients and 17 control subjects (mean age 43 years). In contrast, the sympathoadrenal system (plasma noradrenaline, plasma adrenaline) and renin/aldosterone were significantly activated in decompensated cirrhotics. Circulating ANP was not related to plasma noradrenaline and adrenaline, plasma renin activity, plasma aldosterone, blood pressure, heart rate, or urinary sodium/potassium excretion in any cirrhotic group. Despite established sodium and volume retention in decompensated cirrhosis, the results indicate that diminished effective blood volume fails to release atrial natriuretic peptide in a larger amount due to insufficient atrial stretching. After insertion of a peritoneovenous shunt in one patient for treatment of refractory ascites, plasma atrial natriuretic peptide, urinary volume and sodium excretion increased, whereas elevated plasma levels of noradrenaline, renin activity and aldosterone decreased markedly.
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PMID:Atrial natriuretic peptide in hepatic cirrhosis: relation to stage of disease, sympathoadrenal system and renin-aldosterone axis. 294 55

The acute effects of human atrial natriuretic peptide (ANP) were investigated in 10 patients with liver cirrhosis and ascites. In all patients, diuresis and natriuresis were stimulated with a wide individual variation (50 to 500%) in response to a bolus injection of 30 micrograms ANP. No side effects of treatment were observed. Continuous infusion of ANP (300 micrograms/10 h/d) in a patient with liver cirrhosis and ascites, resistant to conservative forms of diuretic therapy, resulted in an initial increase of diuresis and natriuresis which subsequently returned to pretreatment levels. After initiation of pulsatile nocturnal treatment (5 pulses of 30 micrograms ANP every 3 h), diuresis increased, leading to a persistent normalization of sodium and chloride excretion. The patient lost 8 kg of weight during 16 days of treatment. Out of 3 additional patients on the same therapeutic regime, only one experienced a weight loss of 5 kg due to increased natriuresis and chloruresis. The remaining 2 patients did not respond during 5 resp. 7 days of therapy.
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PMID:Human atrial natriuretic peptide (ANP) for the treatment of patients with liver cirrhosis and ascites. 294 56

Endogenous alpha-atrial natriuretic peptide (ANP) in plasma is elevated in various hypervolaemic conditions. Possible relationships between circulating immunoreactive ANP and cardiovascular and splanchnic haemodynamics were therefore studied in patients with cirrhosis (n = 16) and controls (n = 12). Arterial plasma concentration of ANP in supine patients was (mean +/- SEM) 33 +/- 4 vs 41 +/- 10 pg/ml (9.9 +/- 1.2 vs 12.3 +/- 3.0 fmol/l) in controls (n.s.), and there was a weak direct correlation with right atrial pressure (r = 0.36, P = 0.05). There was no relationship with the presence of ascites or diuretic treatment. Central blood volume (CBV, i.e. the blood volume in the heart cavities, lungs, and aorta), determined from the mean transit time of 125I-labelled of 125I-labelled albumin and cardiac output, was significantly reduced in cirrhotics compared to controls (1.45 +/- 0.12 vs. 1.83 +/- 0.10 l, P less than 0.02) and inversely correlated with portal pressure (r = 0.42, P less than 0.05), whereas total plasma volume was somewhat increased (3.51 +/- 0.2 vs. 3.19 +/- 0.2, 0.05 less than P less than 0.1). A high arterio-venous extraction of ANP was found in the splanchnic system (extraction ratio 0.44 vs 0.28), kidney (0.45 vs 0.54), lower limb (0.53 vs 0.40), and forearm (0.27 vs 0.18) in patients and controls, respectively (n.s.). Our results suggest that the lack of elevation of circulating ANP in cirrhosis, even in the presence of actual fluid retention, may be explained by central hypovolaemia in these patients. Turnover and degradation of ANP is rapid and normal, as evaluated from the tissue extraction ratios.
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PMID:Circulating atrial natriuretic peptide (ANP) and central blood volume (CBV) in cirrhosis. 295 59

The diuretic and natriuretic responses to atrial natriuretic peptide in conscious rats with cirrhosis (chronic bile duct ligation) were examined. Cirrhotic rats had sodium retention, ascites, and elevated liver weights. In conscious control rats, atrial natriuretic peptide increased urine flow rate and urinary sodium excretion. In conscious cirrhotic rats, atrial natriuretic peptide had no effect on urine flow rate or urinary sodium excretion. Renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide in cirrhotic rats. Renal sympathetic nerve activity increased in conscious cirrhotic rats during infusion of atrial natriuretic peptide but decreased in conscious control rats. Inhibition of the renin-angiotensin system with captopril had no effect on the diuretic or natriuretic responses to atrial natriuretic peptide in conscious control or cirrhotic rats. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were affected similarly by atrial natriuretic peptide in control and cirrhotic rats. Increased renal sympathetic nerve activity, but not angiotensin II, mediates the blunted diuretic and natriuretic responses to atrial natriuretic peptide in conscious cirrhotic rats.
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PMID:Renal nerves mediate blunted natriuresis to atrial natriuretic peptide in cirrhotic rats. 295 57

Sodium retention in liver cirrhosis is thought to be due to, among other things, lack of a natriuretic factor or failure to respond to one. alpha-Human-atrial natriuretic peptide is a peptide that accounts partly or entirely for the circulating natriuretic activity in man. In the present study, we have evaluated the effects of the bolus administration of synthetic alpha-human-atrial natriuretic peptide (1 microgram per kg) to patients with liver cirrhosis and variable degrees of sodium retention. alpha-Human-atrial natriuretic peptide induced rapid and marked increases of diuresis and natriuresis in patients without sodium retention or with moderate retention. The results were comparable to those obtained in six healthy control subjects. Conversely, the diuretic and natriuretic effects of alpha-human-atrial natriuretic peptide were attenuated or completely blunted in patients with avid sodium retention. The two groups of patients differed not only in basal sodium excretion, but also in plasma renin activity and in plasma aldosterone levels, suggesting that the reduced responsiveness to atrial natriuretic peptide might be due to excessive antagonism by antinatriuretic factors. The direct relationship between baseline sodium excretion rate and that stimulated by human-atrial natriuretic peptide administration was consistent with this interpretation. In none of the subjects did plasma renin activity peptide and cortisol levels change after human-atrial natriuretic peptide, while plasma aldosterone slightly declined in cirrhotics. Blood pressure fell after the administration of the peptide, with the drug greater in cirrhotic than in normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal response to atrial natriuretic peptide in patients with advanced liver cirrhosis. 296 23

Using a specific radioimmunoassay for atrial natriuretic peptide (ANP), plasma immunoreactive ANP was measured in 17 normal subjects and 83 patients with various diseases. Plasma ANP concentration in normal subjects was 14.1 +/- 1.7 pg/ml (mean +/- S.E.). Relatively high plasma ANP concentrations were detected in patients with diabetes mellitus, hyperthyroidism, atrial fibrillation and liver cirrhosis. Plasma ANP concentrations in the patients correlated positively with mean arterial blood pressure and plasma AVP concentrations. Plasma ANP concentrations in the patients also had positive correlations with left atrial dimension and left ventricular diastolic dimension determined by echocardiography. Another positive correlation was observed in the patients between plasma AVP concentrations and mean arterial blood pressure. These results suggest that ANP is a volume regulatory hormone but also that ANP may be involved in the blood pressure regulating system.
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PMID:Atrial natriuretic peptide and vasopressin in human plasma. 296 44

To assess the role of atrial natriuretic peptide (ANP) in relation to the sympathoadrenal and renin-angiotensin-aldosterone system, and sodium excretion, 88 cirrhotic patients (mean age 52 years; 28 compensated, 28 decompensated with ascites, and 32 decompensated and treated with diuretics) and 26 control subjects were investigated. Basal ANP levels were not different between any group of cirrhotics and controls. Circulating ANP was not related to elevated plasma noradrenaline and adrenaline, and enhanced plasma renin/aldosterone levels in ascitic patients. Furthermore, ANP was not related to urinary sodium excretion, blood pressure, and heart rate. In 30 cirrhotic patients (12 compensated, 18 decompensated with ascites including eight on diuretic therapy) and nine controls, a passive leg rising procedure for 1 h was performed in order to augment central blood volume and atrial pressure physiologically. Ascitic patients (with and without diuretic treatment) experienced a slight but significant increase in plasma ANP indicating preserved responsiveness of ANP release in cirrhosis. Plasma aldosterone was markedly depressed. The data support the underfilling concept of ascitic formation in advanced stages of cirrhosis. The failure of enhanced ANP release under basal conditions may be due to the diminished effective blood volume, resulting in insufficient atrial stretching.
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PMID:Interrelationship between atrial natriuretic peptide and plasma renin, aldosterone and catecholamines in hepatic cirrhosis: the effect of passive leg rising. 297 Jan 63

Plasma levels of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP), and the plasma renin activity (PRA) were examined in 15 vascularly decompensated patients suffering from liver cirrhosis, before and after administration of albumin and after a subsequent administration of furosemide. The initial ANP level was lower in 9 patients (group "A") and higher in 6 patients (group "B") than in healthy controls (Group "A": 19.5 +/- 3.0 fmol/ml; group "B": 36.7 +/- 3.9 fmol/ml; control: 25.8 +/- 2.4 fmol/ml). The initial PRA (4.4 +/- 1.0 ng AngI/ml/h) and AVP (8.5 +/- 1.5 pg/ml) activity in group "A" increased significantly compared to group "B" (PRA: 0.44 +/- 0.09; AVP: 4.1 +/- 0.5), indicating an intravascular volume depletion in group "A". Albumin infusion raised the urine and sodium excretion and the plasma concentration of ANP in group "A" but lowered in plasma levels of renin and vasopressin. The same parameters were not changed by albumin in group "B". Furosemide equally raised the urine flow rate and sodium excretion in both groups. Plasma ANP level depends on the intravascular volume, and the secondary change in its plasma concentration plays a considerable role in the retention of fluid and electrolytes in patients with cirrhosis. The increased intravascular volume in these patients depletes the fluid and electrolyte retention via the increase in ANP level.
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PMID:Alterations of vasoconstrictor and sodium-regulating hormone systems in vascularly decompensated liver cirrhosis. 297 Jun 21

Sensitive radioimmunoassay for determination of immunoreactive atrial natriuretic peptide (ANP) in human plasma was developed and employed for the study of plasma ANP concentrations in healthy controls under basal conditions (2.4 +/- 0.1 pmol/l) and during volume expansion by saline infusion (9.6 +/- 2.0 pmol/l and 14.2 +/- 1.8 pmol/l, respectively). Plasma renin activity and plasma aldosterone concentration exhibited opposite changes during saline infusion. In pathological states associated with extracellular fluid volume (ECFV) expansion, ANP concentration were significantly higher than in the controls (liver cirrhosis 8.6 +/- 0.9; congestive heart failure 33.1 +/- 4.8; chronic renal failure before haemodialysis 72.2 +/- 6.4 pmol/l). Further volume expansion in liver cirrhosis by saline infusion led to the further increase in ANP (13.3 +/- 1.3 and 16.1 +/- 1.5 pmol/l, respectively) and ECFV reduction by ultrafiltration during haemodialysis in chronic renal failure diminished but did not normalize plasma ANP (22.5 +/- 2.9 pmol/l). In patients with arterial hypertension the concentration of ANP exceeded the normal range by 62.5% and reached 8.0 +/- 0.5 pmol/l on the average. Our results support the suggestion that ANP is an important regulatory humoral mechanism participating in the regulation of sodium, volume and blood pressure homeostasis.
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PMID:Radioimmunoassay of atrial natriuretic peptide in human plasma: application to studies of volume and blood pressure homeostasis. 297 15

The plasma levels of atrial natriuretic peptide were determined by radioimmunoassay in 24 patients with chronic liver disease, including three patients with alcoholic liver disease, four with chronic active hepatitis, 13 with liver cirrhosis, and four with hepatocellular carcinoma. When compared with normal subjects (180 +/- 12 pg/ml), the plasma levels of atrial natriuretic peptide in cirrhotic patients (349 +/- 64 pg/ml) were significantly elevated (p less than 0.001) but not in other disease groups. In patients with chronic liver disease the plasma levels of atrial natriuretic peptide were correlated significantly with plasma renin activity but not with plasma aldosterone, and furthermore showed a negative correlation with indocyanine green disappearance rate. These results suggest that the increased plasma levels of atrial natriuretic peptide, which appear to be associated with an increase in plasma renin activity and with hepatic dysfunction, may participate in maintaining homeostasis of sodium and fluid volume in patients with chronic liver disease.
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PMID:Plasma levels of atrial natriuretic peptide in patients with chronic liver disease. 303 81


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