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)

Infusion of the angiotensin-II-antagonist saralasine led in one patient with Bartter's syndrome and one patient with decompensated hepatic cirrhosis, both of whom had a markedly raised plasma renin activity, to a fall in systolic and diastolic blood pressure. The results indicate that in normotensive patients a raised angiotensin II concentration in blood is haemodynamically important for the level of blood pressure if plasma renin activity is raised. In normotensives with normal plasma renin activity saralasine in the usual dosage (4.2 mug/kg-min) does not influence the blood pressure.
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PMID:[The influence of saralasine on blood pressure and renal function in Bartter's syndrome and decompensated hepatic cirrhosis (author's transl)]. 95 92

The electrophoretic mobility of renin substrate in human plasma was determined by electrophoresis of the plasma on a cylinder of polyacrylamide gel, followed by slicing the gel, incubation of each slice with human renin, EDTA, and BAL in saline, and determination of the angiotensin formed by radioimmunoassay. With this modified technique 5, and possibly 8, electrophoretically dissimilar renin substrates have been found in human plasma. Significant variations in the patterns of renin substrates in the blood plasma of pregnant women and of those taking oral contraceptives were shown. In normal plasma from male or female subjects there was a single large peak of renin substrate with a mobility slightly less than that of albumin, and there were a series of very small peaks of renin substrate with lesser mobilities than the major peak. Increasing the sample size and prolonging the period of incubation with renin made the smaller peaks more apparent. In women using oral contraceptives, a distinctly different pattern of renin substrates was found. Early smaller peaks were increased. The major peak was sometimes increased also. Pregnancy produced a strikingly different pattern of renin substrates. There was an increase in all slow-moving peaks and their bases ran together without a return to the baseline. The absence of peaks when renin was omitted indicated that they were renin substrates. In 2 of 4 patients having cirrhosis of the liver with ascites, the amount of major substrate peak was greatly diminished and minor peaks were somewhat reduced. In 3 bilaterally nephrectomized patients, the major peak was not increased and the pattern of minor peaks was normal.
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PMID:Heterogeneity of renin substrate in human plasma: effect of pregnancy and oral contraceptives. 99 64

In order to study the role of renin in regulating blood pressure in normotensive states, saralasin (P113) was infused into normal subjects and patients with cirrhosis of the liver and ascites. In normal subjects on a normal sodium intake, P113 infusion had no effect on blood pressure. Only after the combined stress of a low sodium diet and the upright position did P113 lower the blood pressure. In two of the six cirrhotic patients, P113 caused a significant decrease in BP in the supine position. There was no consistent effect of the P113 infusion on plasma aldosterone or plasma renin activity in the normal or cirrhotic subjects.
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PMID:The role of renin in the control of blood pressure in normotensive man. 101 62

1-Sarcosine, 8-isoleucine angiotensin II (Sar1-Ile8-AII) was infused intravenously in 5 normal volunteers and 66 subjects with various hypertensive, fluid and electrolyte disorders. Changes of blood pressure (BP), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were studied. In normal subjects, Sar1-Ile-AII showed pressor (agonistic) activity, which was related to both dosage and sodium intake. Hyporeninaemic hypertensive subjects (pirmary aldosteronism) showed pressor responses to a smaller dose of this compound than the dose employed in normal subjects. Hyporeninaemic hypertensive subjects and normal volunteers after 3 days of high sodium intake showed significant elevations of BP and PAC and reduction of PRA. Changes of BP, PAC and PRA in normoreninaemic subjects including those with Bartter's syndrome, renal tubular acidosis or liver cirrhosis with ascites showed reduction of BP and PAC and elevation of PRA. The results indicate that the compound has both agonistic and antagonistic activities for blood pressure; which of these is obtained apparently depends upon endogenous angiotensin II levels, as well as the dosage employed. The results in subjects with high and low PRA suggest that the compound has antagonist and agonist actions at 3 sites of angiotensin II action, i.e. peripheral vascular bed, renin release mechanism from juxta-glomerular apparatus and the zona glomerulosa of the adrenals.
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PMID:Changes of blood pressure, plasma renin activity and plasma aldosterone concentration following the infusion of Sar1-Ile8-angiotensin II in hypertensive, fluid and electrolyte disorders. 101 63

The factors involved in renin release have been extensively evaluated. The primary determinants are the transmural pressure at the afferent arteriole, sodium delivery to the macula densa, and the activity of the adrenergic nervous system. Other possible factors include circulating catecholamines, the serum and cerebrospinal fluid sodium concentration, serum potassium concentration, angiotensin II concentration, and antidiuretic hormone release. There is no convincing evidence that the renin-angiotensin system mediates renal autoregulation. Plasma renin activity is altered in a number of clinical settings. This parameter is elevated in most patients with cirrhosis and the nephrotic syndrome as well as in individuals with severe congestive heart failure. Despite inappropriately large weight gains, plasma renin suppresses normally with increased salt intake in edematous patients who have a normal glomerular filtration rate. The mechanisms of the alteration in the renin-angiotensin system in Bartter's syndrome is still not clear.
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PMID:Renin and the kidney. 110 Oct 89

Plasma renin activity and aldosterone metabolism were investigated in patients with cirrhosis and refractory ascites. All patients initially showed marked elevations of plasma and renin activity and plasma aldosterone. Although metabolic clearance of aldosterone was reduced, increased secretion rate was the major factor leading to elevated plasma levels. The elevated plasma renin activity and plasma aldosterone were only minimally affected by posture, dietary sodium restriction, and diuretic administration, suggesting a near-maximal degree of secondary aldosteronism. In most patients plasma renin activity and plasma aldosterone returned to normal when spontaneous natriuresis appeared. However, in 2 patients during spontaneous diuresis and in all 3 given aminoglutethimide, sodium excretion was poorly correlated with plasma renin activity and plasma aldosterone, suggesting that other tubular and/or vascular factors are important in the intense sodium reabsorption found with cirrhosis and ascites.
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PMID:Studies of renin and aldosterone in cirrhotic patients with ascites. 115 87

The protease inhibitor aprotinin was given a) in experimental septic shock, and b) in patients with hepatic cirrhosis and ascites, since in both conditions, activation of the plasma kallikrein-kinin system is associated with pathological systemic vasodilatation, which may trigger reflex neuroendocrine activation and renal solute retention. Given early in experimental sepsis, aprotinin maintained the arterial pressure, systemic vascular resistance (SVR), creatinine clearance and sodium excretion, all of which fell in controls. Aprotinin also blocked increases in pulmonary artery pressure and plasma renin activity (PRA). Given late in sepsis, aprotinin caused a rapid rise in arterial pressure and SVR towards baseline levels. In cirrhosis, aprotinin increased SVR in patients with low baseline values, and improved glomerular filtration rate, renal plasma flow and sodium excretion in all subjects; PRA was suppressed by aprotinin. Aprotinin reverses pathological systemic vasodilatation in these two conditions, and this is associated with a reduction in renin release and improved renal function.
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PMID:Vasoactive effects of aprotinin. 128 72

The IV infusion of pharmacological doses (0.05 microgram.kg-1.min-1) of atrial natriuretic peptide to 16 patients with cirrhosis and ascites induced a significant increase in sodium excretion (65 +/- 23 to 517 +/- 231 mu Eq/min), urine volume (10.7 +/- 2.3 to 15.7 +/- 3.7 mL/min), and glomerular filtration rate (89 +/- 4 to 110 +/- 4 mL/min) in only 5 patients (responders). No significant changes in these parameters (15 +/- 6 to 11 +/- 4 mu Eq/min, 5.5 +/- 1.0 to 4.2 +/- 1.1 mL/min, and 81 +/- 5 to 79 +/- 6 mL/min, respectively) were observed in the remaining patients (nonresponders). Compared with responders, nonresponders had significantly lower baseline sodium excretion (P less than 0.02), urine flow (P less than 0.05), free water clearance (2.5 +/- 0.9 vs. 6.9 +/- 2.1 mL/min; P less than 0.05), and mean arterial pressure (82 +/- 3 vs. 96 +/- 2 mm Hg; P less than 0.01) and significantly higher plasma renin activity (16.3 +/- 4.9 vs. 1.8 +/- 0.2 ng.mL-1.h-1; P less than 0.05) and aldosterone level (99 +/- 24 vs. 13 +/- 2 ng/dL; P less than 0.05). Atrial natriuretic peptide produced a similar reduction of arterial pressure in both groups. To investigate whether the blunted natriuretic response to atrial natriuretic peptide in nonresponders was caused by their lower arterial pressure, atrial natriuretic peptide was infused in 7 of these patients after increasing their arterial pressure to the levels of responders with nonrepinephrine. The increase in arterial pressure (from 81 +/- 5 to 95 +/- 5 mm Hg), which was not associated with significant changes in plasma renin activity and aldosterone concentration, did not reverse the blunted renal response to atrial natriuretic peptide in any of these patients. These results indicate that cirrhotic patients with blunted renal response to atrial natriuretic peptide are characterized by low arterial pressure, marked overactivity of the renin-aldosterone system, and severe sodium and water retention. Correction of hypotension without increasing effective blood volume does not restore renal insensitivity to atrial natriuretic peptide.
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PMID:Renal insensitivity to atrial natriuretic peptide in patients with cirrhosis and ascites. Effect of increasing systemic arterial pressure. 142 99

The "Peripheral Arterial Vasodilation" hypothesis most completely explains the clinical spectrum of cirrhosis ranging from compensated to decompensated to the hepatorenal syndrome (Figure 15-1). As the systemic peripheral vasodilation increases, the neurohumoral responses to arterial underfilling are stimulated with resultant renal vasoconstriction, sodium and water retention. Hypoalbuminemia and portal hypertension, as well as local effects of vasodilation at the capillary level, also contribute to ascites formation and peripheral edema. The suppressed plasma renin activity and aldosterone concentrations and exaggerated natriuresis, which are observed in some patients with early cirrhosis during HWI and the supine position, probably indicate greater central translocation of splanchnic fluid in these volume expanded cirrhotic patients when compared with normal subjects. This interpretation is supported by the greater increases in ANF during HWI in these patients when compared with controls. The neurohumoral responses to arterial vasodilation in cirrhosis combine to decrease distal sodium and water delivery, an event which impairs escape from the sodium retaining effects of aldosterone and causes resistance to the distal tubular effect of ANF (Figure 15-3). As discussed, the peripheral arterial vasodilation of cirrhosis is no doubt multifactorial in nature and the resultant arterial underfilling may be worsened by events that could impair the cardiac response to afterload reduction, including bile salt accumulation, alcoholic cardiomyopathy, and tense ascites decreasing cardiac preload. This pathogenetic schema of cirrhosis is compatible with the unifying body fluid volume hypothesis (Figure 15-3), which we have recently proposed.
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PMID:Pathogenesis of sodium and water retention in liver disease. 129 35

To investigate the renal effects of somatostatin in cirrhosis, renal function and plasma and urinary levels of endogenous neurohumoral vasoactive substances were measured in conditions of intravenous water overload (20 mL/kg body wt with 5% glucose) before and during the intravenous infusion of somatostatin (250-500 micrograms/h) in 6 cirrhotic patients without ascites and 17 nonazotemic cirrhotic patients with ascites. Somatostatin induced a significant reduction of renal plasma flow, glomerular filtration rate, and free water clearance in both groups of patients. In patients with ascites, somatostatin also reduced urinary sodium excretion. Changes in renal function were significantly more marked in patients with ascites than in those without ascites and occurred in the absence of changes in mean arterial pressure and plasma levels of renin, aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic peptide. Somatostatin induced a significant reduction in the plasma concentration of glucagon and urinary excretion of prostaglandin E2 that was not related to changes in renal function. These findings indicate that somatostatin administration induces renal vasoconstriction and impairs glomerular filtration rate, free water clearance, and sodium excretion in cirrhosis by a mechanism unrelated to systemic hemodynamics and endogenous neurohumoral vasoactive systems.
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PMID:Effects of somatostatin on renal function in cirrhosis. 809 52


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