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

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.
 ...
PMID:Atrial natriuretic factor and its role in the regulation of electrolyte, volume and pressure homeostasis. 252 70

Insulin-like growth factor II is secreted primarily by the liver and is reported to be transcribed in many primary hepatocellular carcinoma (PHC) cell lines. We have studied diagnostic significance of serum IGF-II in chronic liver diseases using specific enzyme immunoassay. Serum IGF-II levels (mean +/- SE) were decreased in chronic hepatitis (538 +/- 51 ng/ml; N = 29), liver cirrhosis (427 +/- 45; 50) and PHC (260 +/- 41; 17) compared to controls (830 +/- 49; 57). Serum IGF-II was not different from controls in any of nonhepatic diseases such as diabetes (1032 +/- 97; 19) pancreatic cancer (1413 +/- 282; 8), chronic pancreatitis (999 +/- 126; 17), peptic ulcer (1186 +/- 43; 11), irritable bowel syndrome (1002 +/- 109; 12), gastrointestinal tract cancer (1250 +/- 216; 21) and chronic renal failure (733 +/- 135; 14). In liver diseases serum IGF-II showed a significant correlation with liver function test (negative with retention of indocyanine green and total bile acids; positive with albumin, thrombo-test, and cholinesterase). These results suggest that serum IGF-II reflects a reduced production of IGF-II in the liver and that it can be an index for the residual capacity of liver function.
 ...
PMID:Serum insulin-like growth factor II in chronic liver disease. 253 15

Plasma pancreastatin (PST)-like immunoreactivity in normal subjects and patients with various diseases was estimated by a RIA, using antiserum raised against a synthetic C-terminal peptide of human PST deduced from the sequence of human chromogranin-A. The mean level +/- SEM was 13.2 +/- 0.6 pmol/L in normal subjects, but was significantly higher in patients with chronic renal failure (526.7 +/- 48.5). An immunoreactive form corresponding to a human PST-like sequence [human chromogranin-A-(250-301)] and a larger form were detected by gel filtration of plasma from these patients, suggesting accumulation of the larger molecular form in these patients. A significant increase in PST-like immunoreactivity was also found in patients with liver cirrhosis (20.8 +/- 3.0 pmol/L), but not in patients with noninsulin-dependent diabetes mellitus, chronic pancreatitis, or pancreatic cancer. Elevated levels were found in 16 of the 21 patients with small cell lung carcinoma examined. High levels were also found in 3 of 11 patients with islet cell tumor.
 ...
PMID:Plasma pancreastatin-like immunoreactivity in various diseases. 255 88

Chronic diseases (diabetes mellitus, end stage renal failure on hemodialysis, post-hepatitic liver cirrhosis) caused autonomic neuropathy in 34 of 65 cases. The frequency of autonomic neuropathy was 14 of 30 diabetics (typ I and typ II), twelve of 19 patients on dialysis, and eight of 16 non-alcoholic liver cirrhotics. We did not find a correlation between the tests of the cardiovascular and of the gastrointestinal system. The distribution of the neuropathic changes was undependent of the underlying disorder. Using appropriate tests, alterations of the autonomic functions can be discovered frequently even in asymptomatic patients. At least two pathological test results are necessary to reach a significant difference between patients and healthy controls. This indicates that the diagnosis of autonomic neuropathy should rely on two or more pathological test results. The evidence of autonomic neuropathy identifies a population of high risk patients.
 ...
PMID:[Autonomic neuropathy in diabetes mellitus, chronic renal failure and liver cirrhosis]. 271 53

The neurological disorders seen in patients with chronic renal failure and liver cirrhosis are analogous. Previous in vivo studies have shown that the impaired blood-brain amino acid transport seen in rats with chronic renal failure is similar to that of rats with portocaval anastomosis. To elucidate whether a comparable underlying pathogenic mechanism plays a role in both pathological conditions, blood and brain amino acid levels together with amino acid transport by isolated brain microvessels have been studied in rats with chronic renal failure and in sham-operated rats. Brain microvessels isolated from rats with experimental chronic renal failure showed that the uptake of labeled large neutral amino acid, i.e., leucine or phenylalanine, but not of lysine or alpha-methylaminoisobutyric acid, was significantly increased with respect to sham-operated rats; conversely, the uptake of glutamic acid in rats with chronic renal failure was significantly lower compared with values in controls. Kinetic analysis indicated that this was mainly due to increased exchange transport activity (Vmax) of the L-system, rather than to changes in the affinity (Km) of the carrier system for the relative substrate. These data, together with the significant rise of brain glutamine levels and an increased brain-to-plasma ratio of the sum of large neutral amino acids, are analogous to what was previously observed in rats with portocaval anastomosis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Uptake of amino acids by brain microvessels isolated from rats with experimental chronic renal failure. 290 21

Plasma immunoreactive methionine enkephalin is increased in cirrhosis. To determine whether it was increased in acute liver disease and chronic renal failure and whether the peptide was present in bile and urine, it was measured by radioimmunoassay in appropriate samples. Plasma immunoreactive methionine enkephalin, while at its peak in 15 patients with acute liver disease (median 425 pmol/l, range 220-1460), was approximately six times greater (P less than 0.001) than in 15 patients with chronic renal failure (70 pmol/l, 50-140), 15 controls with other diseases (75 pmol/l, 50-115) and 15 healthy controls (65 pmol/l, 50-95). In eight of the patients recovering from acute liver disease, the decline of the peptide's plasma level correlated with that of the alanine aminotransferase (r = 0.813, P less than 0.01) and prothrombin time (r = 0.682, P less than 0.05) measured in the simultaneously taken blood. Immunoreactive methionine enkephalin was found to be excreted in bile and urine. The possibility that increased plasma methionine enkephalin, and possibly other opioid peptides, may contribute to some of the manifestations of acute liver failure is worthy of further investigation.
 ...
PMID:Methionine enkephalin is increased in plasma in acute liver disease and is present in bile and urine. 292 3

A sensitive and specific radioimmunoassay for alpha-human atrial natriuretic polypeptide (alpha-hANP) was developed to determine its plasma level. Anti-alpha-hANP rabbit serum was specific for the N-terminus and ring structure of alpha-hANP, and showed no appreciable cross-reactions with other neuropeptides. The lowest level of alpha-hANP detectable by this radioimmunoassay was 4 pg per tube. The intra- and inter-assay coefficients of variation were 4.6-11.4% and 7.9-11.8%, respectively, and the recovery rates at 4 concentrations were 62.6-74.0%. The fasting plasma alpha-hANP concentration in normal subjects were 19.3 +/- 1.0 ng/l (mean +/- SE; n = 54), and there was no sex difference. The plasma alpha-hANP level in normal subjects fell significantly during water deprivation and increased significantly on infusion of hypertonic saline. The mean plasma levels of alpha-hANP were higher than normal in patients with essential hypertension, liver cirrhosis, congestive heart failure and chronic renal failure. Our results indicate that this radioimmunoassay is suitable for determining the alpha-hANP concentration in human plasma and can assess changes in pathological and physiological states.
 ...
PMID:Radioimmunoassay for atrial natriuretic peptide: method and results in normal subjects and patients with various diseases. 294 73

Using RIAs for the N- and C-terminal fragments of the human atrial natriuretic polypeptide (ANP) precursor gamma ANP, that is gamma ANP-(1-25), and alpha ANP [gamma ANP-(99-126)], we studied the secretion of gamma ANP-derived peptides from the heart in normal subjects and patients with heart disease, chronic renal failure, and cirrhosis. We detected gamma ANP-(1-25)-like immunoreactivity (-LI) in plasma from normal subjects (n = 17) in considerable amounts [mean, 510 +/- 62 (+/- SE) pg/mL (174 +/- 21 pmol/L)]; the mean plasma alpha ANP-LI level at the same time in these subjects was 32.8 +/- 4.4 pg/mL (10.7 +/- 1.4 pmol/L). Gel permeation chromatographic analysis of plasma samples from normal subjects and patients with heart disease and chronic renal failure revealed two major components; one was alpha ANP, and the other was the 10K N-terminal gamma ANP fragment (N-peptide) resulting from the removal of alpha ANP (3K) from gamma ANP (13K). In addition, gamma ANP (13K), which possessed both gamma ANP-(1-25)-LI and alpha ANP-LI, and beta ANP, an antiparallel dimer of alpha ANP, were detected in some patients as minor components. A significant positive correlation between plasma levels of the N-terminal gamma ANP fragment and alpha ANP (P less than 0.01) and almost equal step-ups in the coronary sinus plasma levels of the N-terminal gamma ANP fragment and alpha ANP suggest that they are cosecreted in equimolar amounts. The high molar ratio of plasma gamma ANP-(1-25)-LI to alpha ANP-LI (17.4 +/- 1.4) in normal subjects and the significantly higher ratio in patients with chronic renal failure (36.9 +/- 7.1; P less than 0.01) suggest the slower clearance of the N-terminal gamma ANP fragment than alpha ANP and a role for the kidney in its degradation. Since the molar ratio of plasma gamma ANP-(1-25)-LI to alpha ANP-LI in patients with cirrhosis (20.7 +/- 2.7) was similar to that in normal subjects, it is unlikely that the N-terminal gamma ANP fragment is metabolized by the liver. In patients with heart disease, plasma gamma ANP-(1-25)-LI and alpha ANP-LI levels were higher in those with cardiac decompensation and were positively correlated with right atrial pressure, pulmonary arterial pressure, and pulmonary capillary wedge pressure, indicating cosecretion of the N-terminal gamma ANP fragment and alpha ANP in response to atrial stretch.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Gamma-atrial natriuretic polypeptide (gamma ANP)-derived peptides in human plasma: cosecretion of N-terminal gamma ANP fragment and alpha ANP. 297 Apr 70

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.
 ...
PMID:Radioimmunoassay of atrial natriuretic peptide in human plasma: application to studies of volume and blood pressure homeostasis. 297 15

The effects of polyunsaturated fatty acids (phosphatidylcholine) on renal function in healthy subjects and in patients with chronic renal failure, with liver cirrhosis, and with heart failure were studied. The drug was administered at 3.5 mg/kg i.v. (Linoleic acid 1.24 mg/kg). In all cases, the administration of the drug caused an increased excretion of sodium and especially of water with a reduction in basal urinary hypertonicity. The polyuria was caused by the higher glomerular filtration rate not being counterbalanced by an increase in tubular water reabsorption. The water reabsorption was mostly anisosmotic. The presence of urinary hypertonicity excluded an inhibition of ADH secretion by this drug. The sodium excretion was probably caused by an increase of the glomerular filtration rate whereas no significant changes in the tubular reabsorption of sodium were seen. We found a significant (p 0.05) increase in PGE2 urinary excretion after phosphatidylcholine administration. Lysine - acetylsalicylate injection after phosphatidylcholine, in other trials in the same patients, prevented the effects previously reported. Therefore we suggest that the effects of this drug are mediated by an increased availability of renal prostaglandins.
 ...
PMID:Effects of polyunsaturated fatty acids and prostaglandin synthesis on renal function. 308 1


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>