Pentoprilat is a member of a series of l-glutarylindoline-2(S)-carboxylic acid derivatives. Pentopril was evaluated as an inhibitor of a cell-free preparation of angiotensin-converting enzyme (ACE) isolated from rabbit lung. Intravenous administration of incremental doses of pentopril to anesthetized normotensive rats produced a dose-related inhibition of angiotensin I (AI) pressor responses. The onset of inhibition of the A1 pressor response was rapid, and substantial inhibition occurred at 5 min after administration of the ACE inhibitors. Pentopril hydrolyzed in vivo to the biologically active free-acid form of CGS 13934. It was well tolerated in normal volunteers and hypertensive patients. Pentopril was developed for the treatment of both hypertension and congestive heart failure. Pentopril produced little clinical improvement and no biochemical improvement in a patients with rheumatoid arthritis.
Pentoprilat
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产品编号 T68616Cas号 82950-75-2
Pentoprilat is a member of a series of l-glutarylindoline-2(S)-carboxylic acid derivatives. Pentopril was evaluated as an inhibitor of a cell-free preparation of angiotensin-converting enzyme (ACE) isolated from rabbit lung. Intravenous administration of incremental doses of pentopril to anesthetized normotensive rats produced a dose-related inhibition of angiotensin I (AI) pressor responses. The onset of inhibition of the A1 pressor response was rapid, and substantial inhibition occurred at 5 min after administration of the ACE inhibitors. Pentopril hydrolyzed in vivo to the biologically active free-acid form of CGS 13934. It was well tolerated in normal volunteers and hypertensive patients. Pentopril was developed for the treatment of both hypertension and congestive heart failure. Pentopril produced little clinical improvement and no biochemical improvement in a patients with rheumatoid arthritis.
Pentoprilat is a member of a series of l-glutarylindoline-2(S)-carboxylic acid derivatives. Pentopril was evaluated as an inhibitor of a cell-free preparation of angiotensin-converting enzyme (ACE) isolated from rabbit lung. Intravenous administration of incremental doses of pentopril to anesthetized normotensive rats produced a dose-related inhibition of angiotensin I (AI) pressor responses. The onset of inhibition of the A1 pressor response was rapid, and substantial inhibition occurred at 5 min after administration of the ACE inhibitors. Pentopril hydrolyzed in vivo to the biologically active free-acid form of CGS 13934. It was well tolerated in normal volunteers and hypertensive patients. Pentopril was developed for the treatment of both hypertension and congestive heart failure. Pentopril produced little clinical improvement and no biochemical improvement in a patients with rheumatoid arthritis.
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