Acute effects of captopril on systemic and renal hemodynamics and on renal function in cirrhotic patients with ascites.
The reduction of angiotensin II production by captopril--an angiotensin-converting enzyme inhibitor--could suppress hyperaldosteronism without impairment of renal function and could thereby be useful in the treatment of ascites in patients with cirrhosis. Systemic and renal hemodynamics and renal function were studied in 6 nonazotemic patients with cirrhosis and ascites with a low-sodium diet before and after oral administration of 25 mg of captopril. Cardiac output and renal blood flow did not change significantly after administration of captopril, whereas mean arterial pressure significantly decreased. Systemic and renal vascular resistances were significantly reduced. There was a statistically significant reduction of glomerular filtration rate, filtration fraction, and urinary output. Plasma renin activity significantly increased in all patients after administration of captopril. A statistically significant correlation was found between the decrease in mean arterial pressure and the reduction of glomerular filtration, but no relationship was found between basal values of plasma renin activity and the other observed variations. We concluded that captopril mainly induces hypotension due to an increase in renal vasodilatation in ascitic patients with cirrhosis.[1]References
- Acute effects of captopril on systemic and renal hemodynamics and on renal function in cirrhotic patients with ascites. Pariente, E.A., Bataille, C., Bercoff, E., Lebrec, D. Gastroenterology (1985) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
