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)

Blockade of angiotensin-converting enzyme has been variously reported to increase or to decrease sodium excretion in patients with cirrhosis and ascites. We administered captopril (50-150 mg) to 11 patients with cirrhosis and ascites to determine the effects on blood pressure, renal blood flow and sodium excretion. Plasma renin activity increased and mean blood pressure fell (by 14 mm Hg). Para-aminohippurate clearances increased from 321 +/- 53 to 559 +/- 83 ml/min (P less than 0.005), but inulin clearances were minimally altered (73 +/- 8 to 76 +/- 7 ml/min), suggesting preferential dilation of glomerular efferent arterioles. Despite unchanged glomerular delivery of sodium, urinary sodium excretion fell in all subjects (from 2.70 +/- 1.00 to 0.48 +/- 0.21 mEq/h), urinary volume was reduced (377 +/- 55 to 182 +/- 42 ml/h, P less than 0.005), and the natriuretic effect of furosemide was blunted. The antinatriuretic effect of captopril may be mediated by reduced angiotensin II-mediated sodium excretion, by decreased prostaglandin production, and/or by indirect effects of reduced blood pressure. Captopril impairs rather than promotes sodium excretion.
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PMID:Effects of captopril on renal function in patients with cirrhosis and ascites. 329 15

In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction. Captopril caused an increase in plasma renin activity (p less than 0.005) and a decrease in plasma aldosterone (p less than 0.025) from an elevated baseline, and a moderate drop in systolic (p less than 0.025) and diastolic (p less than 0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r = -0.66, p less than 0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r = 0.49, p less than 0.05 for systolic and r = 0.71, p less than 0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels. The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.
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PMID:Effect of captopril on renin and blood pressure in cirrhosis. 331 47

Several investigators have reported that hepatic metabolism of renin can be altered in pathophysiological states (e.g., high-output heart failure, cirrhosis, acute metal toxicity). The hypothesis that circulating angiotensin II may play a role in regulating renin metabolism by the liver was tested in anesthetized dogs. Captopril (SQ 14255) or an angiotensin II-competitive antagonist [( Sar1-Ile8]angiotensin II) was used for blockade of the renin-angiotensin system in two separate groups of dogs. The administration of captopril resulted in a significant fall in the percent extraction of renin by the liver (P less than 0.01) and in the clearance of renin (P less than 0.05). The group receiving the competitive antagonist and time-control animals showed no significant change in renin extraction or renin clearance by the liver. Our data do not support a role for angiotensin II in the regulation of hepatic metabolism of renin, since experiments utilizing the antagonist failed to produce a change. The mechanism by which captopril alters renin metabolism appears to be independent of its blockade of angiotensin II.
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PMID:Hepatic clearance of renin after angiotensin blockade. 388 84

To examine the possible contribution of the renin-angiotensin-aldosterone system to portal hypertension in patients with cirrhosis of the liver, seven such patients were studied with the hepatic venous catheterization technique, in the basal state, and after the intake of 12.5 to 25 mg of captopril. Hepatic venous wedge pressure was 22 +/- 2 mm Hg in the basal state and fell to 19 to 20 mm Hg at 45 to 90 minutes after the administration of captopril (P less than 0.05 to 0.01). Wedge to free hepatic venous pressure difference (basal 14 +/- 2 mm Hg) remained unchanged after captopril, and estimated hepatic blood flow was unaltered. Small but significant reductions in arterial blood pressures were seen after the administration of captopril. Aldosterone concentrations decreased whereas renin activity tended to increase after captopril. It is concluded that captopril inhibits the renin-angiotensin system in patients with cirrhosis of the liver, but fails significantly to decrease portal venous pressure. Captopril is thus unlikely to favorably influence the incidence of bleeding in these patients.
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PMID:Effects of captopril on hepatic venous pressure and blood flow in patients with liver cirrhosis. 632 87

Compared to healthy humans in most patients with cirrhosis and renal sodium and water retention, effects of atrial natriuretic peptide (ANP) on sodium and water excretion are reduced. It has been postulated that this impaired response to ANP is caused by renal vasoconstriction, induced by high levels of angiotensin II. To further investigate this issue, we studied renal hemodynamics (glomerular filtration rate, GFR, single nephron GFR, SNGFR, renal blood flow, RBF) and urinary sodium excretion (UNaV) in rats with CCl4-induced cirrhosis of the liver, before and during ANP infusion. The same parameters were determined in cirrhotic rats after a 4-day pretreatment with the angiotensin-converting enzyme (ACE) inhibitor captopril before and during ANP. Results were compared to those obtained in 2 control groups of healthy rats, one of them pretreated with captopril. Rats with cirrhosis had a significantly reduced GFR, SNGFR, RBF, UNaV and an elevated plasma renin activity compared to healthy controls. ANP caused a significant rise in UNaV (+198%) but no significant change of GFR, SNGFR and RBF in cirrhotic rats. Captopril-pretreated rats with cirrhosis had a significantly higher RBF (+26%) and 24-hour urinary sodium excretion (+52%) but no significant differences in GFR and SNGFR compared to cirrhotic rats without captopril pretreatment. Administration of ANP to cirrhotic rats pretreated with captopril resulted in a significant rise in GFR (+56%), SNGFR (+42%), RBF (+29%) and UNaV (+159%) compared to cirrhotic rats with ANP alone. In healthy rats, there was no additional effect of a combined therapy with captopril and ANP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of atrial natriuretic peptide in cirrhotic rats with and without captopril pretreatment. 832 62