REVIEW Benazeprilat, the active metabolite of Benazepril, competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion. Benazeprilat may also act on kininase II, an enzyme identical to ACE that degrades the vasodilator bradykinin.
Chan KK, Buch A, Glazer RD, John VA, Barr WH: Site-differential gastrointestinal absorption of benazepril hydrochloride in healthy volunteers. Pharm Res. 1994 Mar;11(3):432-7.
De Feo P, Torlone E, Perriello G, Fanelli C, Epifano L, Di Vincenzo A, Modarelli F, Motolese M, Brunetti P, Bolli GB: Short-term metabolic effects of the ACE-inhibitor benazepril in type 2 diabetes mellitus associated with arterial hypertension. Diabete Metab. 1992 Jul-Aug;18(4):283-8.
Gengo FM, Brady E: The pharmacokinetics of benazepril relative to other ACE inhibitors. Clin Cardiol. 1991 Aug;14(8 Suppl 4):IV44-50; discussion IV51-5.
Hou FF, Zhang X, Zhang GH, Xie D, Chen PY, Zhang WR, Jiang JP, Liang M, Wang GB, Liu ZR, Geng RW: Efficacy and safety of benazepril for advanced chronic renal insufficiency. N Engl J Med. 2006 Jan 12;354(2):131-40.
These chemical products are for research and development use only. They are not for diagnostic, therapeutic, cosmetic, or human and animal uses. They are not sold to individuals. Additional restrictions may apply.
New customers undergo an internal onboarding process. As part of this process, new customers may be asked for more information.