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Effects of captopril on renal function in patients with cirrhosis and ascites
Insights
Captopril, an angiotensin-converting enzyme inhibitor, was studied in cirrhosis patients with ascites. Contrary to some reports, captopril impaired sodium excretion and reduced urine volume, indicating an antinatriuretic effect.
Area of Science:
- Nephrology
- Gastroenterology
- Pharmacology
Background:
- Patients with cirrhosis and ascites exhibit variable responses to angiotensin-converting enzyme (ACE) inhibitors regarding sodium excretion.
- Understanding the renal effects of ACE inhibitors in this population is crucial for managing fluid balance.
Purpose of the Study:
- To investigate the impact of captopril on blood pressure, renal hemodynamics, and sodium excretion in patients with cirrhosis and ascites.
- To clarify the net effect of ACE inhibition on sodium balance in this clinical setting.
Main Methods:
- Administration of captopril (50-150 mg) to 11 patients with cirrhosis and ascites.
- Monitoring of blood pressure, plasma renin activity, para-aminohippurate (PAH) and inulin clearances, and urinary sodium and volume excretion.
- Assessment of the interaction with furosemide's natriuretic effect.
Main Results:
- Captopril administration led to a significant fall in mean blood pressure (14 mm Hg) and increased plasma renin activity.
- Para-aminohippurate clearance increased, suggesting efferent arteriolar dilation, while inulin clearance remained largely unchanged.
- Despite stable glomerular sodium delivery, urinary sodium excretion and volume significantly decreased in all subjects.
- The natriuretic response to furosemide was diminished following captopril administration.
Conclusions:
- Captopril demonstrates an antinatriuretic effect in patients with cirrhosis and ascites, contrary to some previous findings.
- This effect may be attributed to reduced angiotensin II activity, decreased prostaglandin synthesis, or indirect blood pressure effects.
- Captopril impairs, rather than promotes, sodium excretion in this patient group.
Abstract:
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.