Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In patients with chronic liver disease a dissociation of the two most important partial functions of the adrenal cortex may be observed. A widening of the zona glomerulosa is associated with an increased aldosterone secretion and an atrophy of the zona fasciculata with a decreased cortisol production rate. In acute alcoholic liver damage there are sometimes remarkable special features concerning the adrenal function. The pathogenesis of the altered C21-steroid hormone metabolism is nonuniform and depends upon the etiology of the liver disease. Following factors may play role: 1. Decreased activity of specific hepatic enzymes a)direct enzyme damage b)indirect enzyme activity decreasing processed by deficiency of hydrogen from NADPH 2. Decreased hepatic blood flow 3. Disturbance of intracellular transport of substrates (e.g. cholestasis 4. Changes of transport proteins. 5. Direct or reactive changes of other factors of hormonal feedback systems (hypothalamus-pituitary-adrenal or gonadal-system; renin-angiotensin-aldosterone-system).
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PMID:Glucocorticoid and mineralocorticoid hormones in chronic liver diseases. 22 7

Fifteen patients with chronic liver disease having a peritoneovenous shunt for chronic intractable ascites were studied prospectively for renal function and hemodynamic changes during balance studies, pre-, peri-, and postoperatively. Shunt insertion caused a rapid redistribution of ascites into the intravascular compartment with hemodilution and significant rises in cardiac output (9 patients) (P less than 0.025) renal blood flow (3 patients) (P less than 0.025), and creatinine clearance (15 patients) (P less than 0.005), and decreases in plasma renin activity (10 patients) and serum aldosterone levels (9 patients) (P less than 0.025). Despite these changes, small repeated doses of furosemide were required to start and maintain a diuresis and natriuresis with sodium excretion rising from 7.2 +/- 4.1 to 174 +/- 44 meq/day (P less than 0.0005) in the 15 patients. At 2 wk postoperatively, the 15 patients had lost a mean of 7.5 kg in weight associated with a persistent improvement in creatinine clearance and a continued natriuresis, 15.9 +/- 7 mEq/day (P less than 0.005), despite no statistically significant change in cardiac output (7 patients) or renal blood flow (4 patients) compared with preoperative levels. This operation is an effective therapy for refractive ascites, but the incidence of potentially fatal complications makes us hesitate to recommend it except for patients resistant to normal conservative measures.
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PMID:The renal and hemodynamic effects of the peritoneovenous shunt for intractable hepatic ascites. 44 39

Prostaglandins may modulate renal function and play a role in the hyperreninism and angiotensin pressor resistance of chronic liver disease. To study this possibility, we evaluated 12 patients with alcoholic cirrhosis and ascites. Urine immunoassayable prostaglandin E in 5 female patients was 3.3 +/- 0.5 micrograms/day [normal, 0.3 +/- 0.1 (SE)], renin was 14.6 +/- 3.7 ng/ml.h, and aldosterone was 76 +/- 19 ng/dl. After either indomethacin (200 mg) or ibuprofen (2000 mg) for 1 day, urine immunoassayable prostaglandin E fell to 0.8 +/- 0.4 micrograms/day, renin to 8.0 +/- 2.4 ng/mol.h, and aldosterone to 54 +/- 14 ng/dl (all P less than 0.01). Pressor sensitivity increased dramatically, and creatinine clearance transiently fell from 73 +/- 10 to 32 +/- 7 cc/min (P less than 0.01). Because a primary effect on renin might explain the renal impairment, an additional study used propranolol to lower renin activity. Renal function was unaltered by propranolol. We conclude that prostaglandins play a supportive role in maintaining renal function and are involved in the hyperreninism and pressor resistance of patients with liver disease.
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PMID:Prostaglandins: modulators of renal function and pressor resistance in chronic liver disease. 44 95

The renin substrate angiotensinogen (AGT) belongs to a supergene family of proteins that also includes alpha 1-antitrypsin (AAT) and alpha 1-antichymotrypsin (ACT), acute-phase reactants with known serine proteinase inhibitory (serpin) function. AGT lacks a known inhibitory function but is an acute-phase reactant. In this study we have compared the plasma levels, as analysed by electroimmunoassay, of AGT with AAT in patients with different types of chronic liver disease. AAT levels are regularly elevated in liver disease patients in contrast to AGT, which remains normal until late in the disease course. The AGT levels (mean +/- SD) were: in alcoholic cirrhosis (n = 19) 100 +/- 27.3%, in chronic active hepatitis (n = 14) 100 +/- 23.2%, in primary biliary cirrhosis (n = 18) 106 +/- 26.1% and in non-alcoholic cirrhosis (n = 15) 92 +/- 38.4%. Only occasionally were levels less than 50% of normal seen. In general, AGT levels were unrelated to sex and type of underlying liver disease and did not correlate with degree of hepatocellular impairment. Crossed immunoelectrophoresis showed no abnormal charge heterogeneity of AGT in patients with low levels. Our data are consistent with a dissociate expression of the homologous serpin genes in chronic liver disease. We speculate that the magnitude of the dissociated response is influenced by hormonal factors.
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PMID:Angiotensinogen in chronic liver disease. 159 89

The discovery of biologically active peptides in mammalian atria represents an important advance in the area of cardiovascular and renal research. Atrial natriuretic factor has been isolated from atrial cardiocytes and is released into the blood after atrial stretch. It has been shown to possess important physiologic actions affecting renal hemodynamics and electrolyte excretion, smooth muscles, blood pressure and the renin-angiotensin-aldosterone system. Its participation in the pathophysiology of congestive heart failure, arrhythmia, hypertension, chronic renal failure and chronic liver disease is reviewed.
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PMID:[Atriopeptin: a new hormone in water-salt regulation]. 215 6

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

The aim of this study was to determine whether hyperreninemia in the adrenalectomized (ADX) rat is dependent on renal prostaglandin synthesis, as has been suggested for two other hyperreninemic conditions, Bartter's syndrome and chronic liver disease. Plasma renin concentration (PRC) in anesthetized, ADX rats was significantly increased (delta +480%; p less than 0.001) compared to sham-operated controls. In vivo, indomethacin (10 mg/kg i.v.) significantly reduced PRC of anesthetized, ADX rats after both 45 min (delta -34%; p less than 0.05) and 90 min (delta -47%; p less than 0.05). In vitro renin release from renal cortical slices of ADX rats was also significantly greater (delta +130%; p less than 0.05) than from sham-operated control cortical slices. Renin release from cortical slices of ADX rats given dexamethasone (10 micrograms/kg/day) for 4 days prior to sacrifice did not differ from sham-operated control values. Prostaglandin E2 (PGE2) release from cortical slices of ADX rats did not differ significantly from controls. However, PGE2 synthesis in glomeruli microdissected from ADX rats was significantly increased (delta +110%; p less than 0.001) compared to controls. PGE2 synthesis in glomeruli of dexamethasone-treated ADX rats remained significantly elevated compared to controls. Ibuprofen (10(-6) M) decreased PGE2 synthesis in cortical slices by 80%. However, prostaglandin synthesis inhibition had no effect on renin release from either ADX or control renal cortical slices. These results suggest that despite increased glomerular synthesis, prostaglandins do not directly influence renin release in the ADX rat.
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PMID:Dissociation of hyperreninemia and renal prostaglandin synthesis in the adrenalectomized rat. 351 58

Furosemide occasionally causes azotemia in patients with ascites, independently of induced volume depletion. To define this effect, we measured renal clearances in patients with chronic liver disease and ascites and in nonascitic controls. Furosemide (80 mg i.v.) transiently increased p-aminohippurate clearance in controls (from 693 +/- 67 to 928 +/- 93 ml/min) and in 11 patients with ascites (from 418 +/- 81 to 526 +/- 80 ml/min). In contrast, in 13 patients with ascites, p-aminohippurate clearance fell by 34% (from 545 +/- 51 to 360 +/- 24 ml/min) within 20 min and by 41% within 60 min, and inulin clearance fell by 19% at 20 min and by 30% at 60 min. The renal effects lasted approximately 4 h. The renal response could not be predicted by renin activity, urinary prostaglandin excretion, urinary sodium, or clinical characteristics. In all 14 patients who received oral furosemide, p-aminohippurate clearance fell within 90 min (by 24%) and remained suppressed for at least 4 h. These immediate effects of furosemide on renal perfusion may contribute to azotemia in some patients with ascites.
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PMID:Immediate effects of furosemide on renal hemodynamics in chronic liver disease with ascites. 356 60

Propranolol hydrochloride is reported to lower portal pressure and inhibit renin secretion in patients with chronic liver disease, actions that might lessen the tendency to ascites formation. We compared the effect of diuretics with that of the same dose of diuretics plus propranolol on natriuresis, urine output, and daily weight loss in 13 hospitalized patients with stable chronic liver disease, sodium retention, and ascites. The propranolol hydrochloride dose was 20 to 160 mg four times a day, titrated to reduce resting pulse by 25% or systolic BP 10 mm Hg. Diuretics given were furosemide, 80 to 160 mg, and triamterene, 100 or 200 mg/day. Periods of time when each regimen was received ranged from one to four days. Creatinine excretion documented complete urine collections. Compared with diuretics alone, diuretics plus propranolol substantially reduced resting pulse, systolic BP, and urine sodium excretion, although not creatinine clearance. This antinatriuretic effect may limit the proposed usefulness of propranolol for prevention of variceal bleeding in patients with cirrhosis and ascites.
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PMID:Propranolol in the treatment of cirrhotic ascites. 647 94

Intestinal secretion and intercullular space dilatation can be induced in animal models by acute elevation of intravascular volume or portal pressure. We examined whether patients with increased portal venous pressure might represent a clinical counterpart to these animal models. Portal venous pressure, determined by hepatic wedge pressure measurement, was elevated to 10-55 mmHg (mean 29 mmHg) in 8 patients with chronic liver disease without diarrhea. Intestinal transport studies utilizing a steady-state perfusion technique revealed normal absorption of a plasmalike electrolyte solution. A solution dsigned to unmask intestinal secretion demonstrated no difference from control subjects in the movement of water, electrolytes, or protein into the intestional lumen. There was no correlation of absorption of secretion with hepatic wedge pressure. Jejunal biopsy revealed a significant increase in dilatation of intercellular spaces in patients compared to controls; this increase was not correlated with hepatic wedge pressure, but was significantly inversely correlated to plasma renin and aldosterone concentration. We conclude that patients with chronic liver disease and portal hypertension absorb water and electrolytes normally, but have mild morphologic alterations in the intestinal mucosa, possibly related to intravascular volume status.
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PMID:Water and electrolyte movement and mucosal morphology in the jejunum of patients with portal hypertension. 740 88


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