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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Passive and carrier-mediated intestinal absorption components of captopril.

The intestinal absorption mechanism of captopril was investigated in fasted rats using a single-pass perfusion method. Captopril and captopril disulfide were analyzed by HPLC. A modified boundary-layer solution was applied to determine the apparent intestinal wall permeabilities (Pw*). The results indicated that captopril is very permeable in the small intestine but not in the colon, and the permeability in the small intestine is both pH and concentration dependent. The estimated parameters for the carrier are: Km*, 6 mM; Jmax*, 12 mM; and Pc*, 2. There is also a significant passive component to captopril absorption in the small intestine. Furthermore, the intestinal permeability of captopril was significantly decreased by the withdrawal of sodium from the perfusate (3 times), and the addition of 85 mM of gly-gly (2.5 times), 15 mM of gly-pro (4 times), dipeptide mixture (4.5 times), 0.5 mM of 2,4-dinitrophenol (4 times), and 10 mM of cephradine (6 times). This is the first demonstration that an angiotensin converting enzyme (ACE) inhibitor is at least in part transported by a carrier-mediated process in the intestine via the peptide carrier system. In addition, the results showed that the peptide carrier system can transport a substrate without a "N" terminal nitrogen atom.[1]


  1. Passive and carrier-mediated intestinal absorption components of captopril. Hu, M., Amidon, G.L. Journal of pharmaceutical sciences. (1988) [Pubmed]
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