Effects of @entity71851 XXXX on tissue angiotensin-converting enzyme in @entity35 .

@entity35 @entity71851 @entity460 @entity1811 @entity551
Tissue angiotensin-converting enzyme ( @entity1811 ) inhibition was measured in @entity35 after single intravenous (i.v.) and oral (p.o.) doses of @entity71851 @entity460 , and the correlation between peak inhibition and tissue concentration of the drug was investigated. Five minutes after @entity71851 @entity460 (3 mg/kg i.v. as free acid), @entity1811 in the examined tissues (serum, lungs, kidneys, heart, aorta, adrenals, testes, and brain) showed > 50% inhibition, always associated with measurable amounts of @entity71851 . After 90 min, @entity1811 activity was still inhibited only in serum, lungs, kidneys, and aorta, recovering to basal values by 8 h in all samples but serum. Oral @entity71851 @entity460 (30 mg/kg) produced > 50% peak @entity1811 inhibition in serum, lungs, and kidneys, in which measurable levels of the drug were detected, and in the aorta, where @entity71851 was not detected. Other tissues showed neither marked inhibition nor measurable drug levels. Kinetics of @entity1811 inhibition in affected tissue mirrored those observed after intravenous administration. @entity71851 , despite its hydrophilic nature, is able to reach extravascular tissues and to inhibit local @entity1811 . However, in no tissue did the effect on @entity1811 last longer than in serum and the hypothesis of a peculiar role of tissue RAS in determining the @entity551 activity of @entity71851 @entity460 is not supported in @entity35 .
