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)

The potent diuretic and natriuretic properties of atrial natriuretic factor (ANF) suggest that atrial hormones may participate to the regulation of salt and water excretion under physiological conditions. ANF, via the increase of its intracellular second messenger cGMP, has been recently shown to inhibit the apical sodium channel of the inner medullary collecting tubule (IMCD). In addition, ANF inhibits renin and aldosterone synthesis and antagonizes the antinatriuretic effects of angiotensin II. ANF may also contribute to the excretion of free water by inhibiting both the secretion of vasopressin and its antidiuretic action. ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. All these factors could explain the lack of significant natriuretic effect of both endogenous and exogenous ANF in some pathological conditions such as heart failure or liver cirrhosis. ANF may also been concerned in water homeostasis. In addition to the well-known osmoregulatory pathways of water metabolism, we recently found that ANF could be involved in the volume adjustment to acute water intake in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Atrial natriuretic factor and the endocrine control of electrolyte homeostasis. 183 42

Cardiac atria and, under certain circumstances, also ventricles produce and secrete into the circulation atrial natriuretic factor (ANF). ANF exerts a significantly natriuretic, myorelaxant, renin-, aldosterone-, and vasopressin-inhibiting effect and acts as a neurotransmitter in the central and autonomous nervous systems. Expansion of the extracellular volume stimulates secretion of ANF which consequently contributes to renal excretion of sodium and water. The renal effect of ANF is apparently modulated by interaction with other mechanisms. ANF concentration in peripheral blood is the product of its secretion by the heart and degradation by peripheral tissues. In ascitic liver cirrhosis, the decreased splanchnic bed uptake may contribute to the increase in plasma ANF concentration observed. Insufficient production or secretion of ANF are not likely to be the primary etiopathogenic mechanism of arterial hypertension. In the course of development of hypertension, ANF is mobilized as a corrective-adaptive mechanism in an effort to normalize the raised BP, extracellular volume or circulating pressor agents. Through its production of ANF, the heart possess an important endocrine function markedly affecting pressure, electrolyte and volume homeostasis.
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PMID:Role of the heart as an endocrine organ. 184 37

We examined the acute effects of sinorphan, an inhibitor of enkephalinase, on plasma atrial natriuretic factor (ANF) and urinary sodium excretion in cirrhotic patients with ascites. A single oral dose of sinorphan (100 or 30 mg in 11 and 5 patients, respectively) was administered against placebo according to a double blind cross-over protocol. Basal plasma ANF levels varied over a large range between 2.6-79 pmol/L. Sinorphan, at a dose of 100 mg, inhibited 70% of plasma enkephalinase activity 60 min after ingestion and elicited simultaneously an increase in plasma ANF and cGMP levels 1.8 and 1.5 times basal values, respectively. There was a transient increase in sodium urinary output without a change in creatinine clearance over the initial 2-h period following drug administration. An increase in urinary cGMP was also observed on a longer period of 6 h. Plasma aldosterone decreased significantly, but the lowest concentration was reached 1 h later than the peak of plasma ANF. Mean blood pressure and PRA were unmodified. The effects of 30 mg sinorphan on plasma ANF, cGMP, and aldosterone were also significant, but less marked than those of the higher dose. Therefore, enkephalinase inhibition transiently increases sodium urinary excretion in cirrhotic patients with ascites via a mechanism that is likely to imply reduction of ANF catabolism. These results suggest that ANF could play a role in the control of sodium homeostasis in liver cirrhosis with ascites.
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PMID:Effect of sinorphan, an enkephalinase inhibitor, on plasma atrial natriuretic factor and sodium urinary excretion in cirrhotic patients with ascites. 184 6

The renal response to atrial natriuretic factor is blunted in cirrhosis with ascites. This might be due to alterations of renal receptors for atrial natriuretic factor. Therefore density and affinity of glomerular atrial natriuretic factor binding sites of bile duct-ligated rats with ascites (n = 10) and of sham-operated controls (n = 10) were determined. Glomerular atrial natriuretic factor binding sites were identified to be of the B-("biologically active") and C-("clearance") receptor type. Discrimination and quantitative determination of B and C receptors for atrial natriuretic factor were achieved by displacement experiments with atrial natriuretic factor(99-126) or des(18-22)atrial natriuretic factor(4-23), an analogue binding to C receptors only. Density of total glomerular atrial natriuretic factor binding sites was significantly increased in bile duct-ligated rats (3,518 +/- 864 vs. 1,648 +/- 358 fmol/mg protein; p less than 0.05). This was due to a significant increase of C-receptor density (3,460 +/- 866 vs. 1,486 +/- 363 fmol/mg protein; p less than 0.05), whereas density of B receptors was not significantly different in bile duct-ligated rats (58 +/- 11 vs. 162 +/- 63 fmol/mg protein). Affinity of atrial natriuretic factor to its glomerular binding sites did not differ significantly between both groups. These data suggest that an altered glomerular atrial natriuretic factor receptor density could be involved in the renal resistance to atrial natriuretic factor in cirrhosis with ascites.
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PMID:Altered density of glomerular binding sites for atrial natriuretic factor in bile duct-ligated rats with ascites. 184 96

Plasma concentrations of atrial natriuretic factor (ANF) and cyclic 3',5'-guanosine monophosphate (cGMP) were measured in 11 cirrhotic patients with ascites, 11 cirrhotic patients without ascites and 15 control subjects. The following were determined in 15 of the cirrhotic patients and in all the control subjects: blood volume (BV) and furosemide-induced changes in BV, plasma values of ANF, cGMP, angiotensin II (AII), aldosterone (Aldo), arginine vasopressin (AVP) and urinary excretion rates of cGMP, prostaglandin E2 (PGE2), water and sodium. Basal plasma levels of ANF and cGMP were higher in patients with cirrhosis than in controls, but were the same in both groups of cirrhotics (ANF: cirrhosis with ascites 12.7, without ascites 13.4, and in controls 5.8 pmol l-1 (medians); cGMP: 7.7, 7.4 and 4.3 nmol l-1, respectively). BV was less reduced after furosemide in the cirrhotic patients (6.0%) than in the healthy subjects (10.1%), but basal BV did not differ. Urinary sodium excretion rates after furosemide were significantly lower in the cirrhotic patients than in the controls. PGE2 excretion rate increased after furosemide in the cirrhotic patients (0.29 to 0.66 pmol min-1; P less than 0.01) but not in the controls (0.31 to 0.38 pmol min-1). After furosemide ANF and cGMP decreased slightly in both groups whereas AII and Aldo increased; AVP increased in the controls, but not in the cirrhotic patients. In conclusion, plasma values of ANF and cGMP are increased in liver cirrhosis both with and without ascites. This and the elevated PGE2 excretion after furosemide may be compensatory phenomena in order to facilitate renal sodium excretion.
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PMID:Atrial natriuretic factor, cyclic 3',5'-guanosine monophosphate and prostaglandin E2 in liver cirrhosis: relation to blood volume and changes in blood volume after furosemide. 196 25

The plasma levels of atrial natriuretic factor in liver cirrhosis can be affected by various factors, such as ascites, renal function, use of diuretics drugs and dietary sodium intake. Moreover, the influence of high intra-abdominal pressure on cardiac atrial natriuretic factor release in patients with tense ascites has not been investigated. The aim of the present study was to evaluate the circulating levels of atrial natriuretic factor and their relationships to plasma renin activity, aldosterone concentration, and urinary sodium excretion in 45 cirrhotic patients divided into 4 groups: (a) cirrhotics without ascites; (b) nonazotemic cirrhotics with ascites; (c) cirrhotics with ascites and functional renal failure; and (d) cirrhotics with ascites taking diuretics. In some patients with tense ascites, atrial natriuretic factor was also measured after rapid abdominal relaxation by large volume paracentesis. Plasma levels of atrial natriuretic factor obtained in 13 healthy control subjects after 5 days on a 40-50 mEq sodium daily intake were 22.8 +/- 3.3 pg/ml. Mean plasma atrial natriuretic factor levels were normal in patients without ascites (35.1 +/- 11.4 pg/ml) and in those with ascites taking diuretics (27 +/- 9.2 pg/ml), but elevated in patients with ascites not taking diuretics (59.6 +/- 12 pg/ml) and in those with ascites and functional renal failure (58.5 +/- 16.6 pg/ml). These data show that plasma atrial natriuretic factor levels are elevated only in cirrhotic patients who are ascitic and not taking diuretics. In these patients atrial natriuretic factor levels were directly correlated with urinary sodium excretion, even though sodium balance was positive. This could be the consequence of the contrasting effects of antinatriuretic factors, as suggested by the inverse relationships between atrial natriuretic factor and urinary sodium on the one hand and plasma renin activity and plasma aldosterone concentration on the other. Twenty-six patients with tense ascites (12 taking diuretics and 14 not) were treated with rapid large-volume paracentesis (6500 +/- 330 ml of ascitic fluid removed in 168 +/- 16 min). At the end of the procedure, plasma atrial natriuretic factor levels had increased in all patients (from 45.5 +/- 10.1 to 100 +/- 17 pg/ml), whereas plasma renin activity and plasma aldosterone concentration had decreased (from 10.3 +/- 1.6 to 7 +/- 1.3 ng/ml/h, and 1160 +/- 197 to 781 +/- 155 pg/ml, respectively).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Atrial natriuretic factor in cirrhotic patients with tense ascites. Effect of large-volume paracentesis. 213 4

In 12 patients with cirrhosis of the liver (six with ascites) and six controls the authors made catheterizations of the hepatic veins and portal circulation, assessing concurrently the in cardiac output by thermodilution. The patients with ascitic cirrhosis had, as compared with controls, a significantly higher portohepatic gradient, central venous pressure, mean pressure in the pulmonary artery and also pulmonary capillary wedged pressure and a significantly lower mean arterial pressure and systemic vascular resistance. These patients had also, as compared with controls, a significantly higher concentration of ANF (atrial natriuretic factor) in the pulmonary artery (15.89 +/- 2.26 vs. 8.04 +/- 0.97, p less than 0.01) and in the hepatic vein (7.44 +/- 0.44 vs. 3.91 +/- 0.63, p less than 0.01); the difference between ANF concentrations in the peripheral blood stream was not significant (9.52 +/- 2.46 vs. 5.71 +/- 1.24 n. s.). Patients with ascitic cirrhosis of the liver had a significantly higher calculated cardiac production of ANF than controls (24.36 +/- 3.44 vs. 8.12 +/- 2.9, p less than 0.01); the difference in the splanchnic extraction of ANF between patients with ascitic cirrhosis of the liver (0.46 +/- 0.1) and controls (0.51 +/- 0.06) was not significant. The ANF concentration in the pulmonary artery in patients with cirrhosis of the liver correlated significantly with the central venous pressure (r = 0.677, p = 0.02) and the pressure in the pulmonary artery in a wedged position (r = 0.639, p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Atrial natriuretic factor in liver cirrhosis. Relation to hemodynamic parameters]. 213 92

N-terminal (atrial natriuretic factor (ANF) 1-98) and C-terminal (ANF 99-126) fragments of proatrial natriuretic factor (NTA and CTA, respectively) were determined in plasma of healthy subjects adopting different postures and in patients with cirrhosis. Seven healthy subjects were investigated while seated and 30 min after assuming a horizontal position. NTA plasma concentrations increased in subjects in the horizontal position (from 734 +/- 250 (SE) fmol/ml to 902 +/- 227 fmol/ml; p less than 0.05). In contrast, CTA plasma concentrations remained unchanged (9.2 +/- 1.3 fmol/ml vs 8.9 +/- 1.6 fmol/ml). In 10 patients with cirrhosis of the liver, NTA concentrations were markedly (p less than 0.001) elevated compared to 11 healthy subjects (2334 +/- 291 fmol/ml vs 743 +/- 155 fmol/ml). However, there was no difference of CTA plasma levels between cirrhotic patients and healthy subjects (8.7 +/- 1.3 fmol/ml vs 8.2 +/- 0.9 fmol/ml). These data demonstrate changes of the plasma concentration of the N-terminal fragment of proatrial natriuretic factor by posture and in liver disease, in contrast to unchanged levels of the C-terminal fragment.
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PMID:Different behaviour of the N-terminal and C-terminal fragment of proatrial natriuretic factor in plasma of healthy subjects as well as of patients with cirrhosis. 214 Feb 1

To 11 patients with liver cirrhosis (5 with ascites) and 6 controls a one-hour dopamine infusion, 1.5 micrograms/kg/min., was administered. In all before administration of the infusion catheterization of the hepatic veins and lesser circulation was performed with concurrent assessment of the cardiac minute volume by thermodilution, and haemodynamic measurements were repeated also after the dopamine infusion. Before the dopamine administration and after termination of the infusion the plasma renin activity was assessed (PRA), plasma aldosterone, the atrial natriuretic factor (ANF), prolactin and in some patients also plasma catecholamines. Dopamine administration was not associated with an increase of the cardiac output, heart rate or peripheral resistance; the infusion had only purely dopaminergic effects. Plasma prolactin declined after dopamine administration significantly in controls (from 29.17 +/- 7.01 to 11.83 +/- 3.22, p less than 0.05, in patients with liver cirrhosis without ascites) from 18.16 +/- 2.44 to 8.64 +/- 2.01, p less than 0.01) in patients with ascites liver cirrhosis (from 23.5 +/- 9.3 to 15.2 +/- 7.47, p less than 0.05). In the controls after the dopamine infusion PRA suppression occurred (from 2.37 +/- 0.81 to 0.9 +/- 0.27, p less than 0.05), while in patients with compensated liver cirrhosis (from 0.97 +/- 0.41 to 0.85 +/- 0.34, n.s.) and in patients with decompensated liver cirrhosis the PRA did not change significantly either (from 4.56 +/- 1.67 to 5.065 +/- 2.29, n. s.). After the dopamine infusion in none of the investigated patient groups changes of plasma aldosterone and ANF were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of dopamine on hemodynamic and hormonal parameters in liver cirrhosis]. 214 Sep 56

Increased blood volume, atrial size, and plasma concentration of atrial natriuretic factor are described in cirrhosis. Their interrelationships were examined in 17 men with alcoholic liver disease, 7 with and 10 without ascites. Atrial size was determined by two-dimensional echocardiography. Patients with cirrhosis had significantly increased left atrial volume and plasma concentration of atrial natriuretic factor when compared with normal male subjects. Right atrial volume was normal in patients with cirrhosis, as was left ventricular function. Patients with ascites had significantly increased blood volume and plasma atrial natriuretic factor concentration compared with patients without ascites. Left and right atrial volume did not differ between the groups. Blood volume correlated significantly with left atrial volume, which correlated significantly with plasma concentration of atrial natriuretic factor. Cirrhosis is associated with related increases in vascular volume, left atrial size, and plasma atrial natriuretic factor concentration. Increased blood volume probably contributes to the increase in left atrial volume, which is in turn one reason for the elevation of plasma atrial natriuretic factor concentration.
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PMID:Atrial volume in cirrhosis: relationship to blood volume and plasma concentration of atrial natriuretic factor. 214 59


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