Overview
- Sever, P. (1997) J. Hum. Hypertens. 2, S91.
- Mendis, B. and Page, S.R. (2009) Expert Opin. Pharmacother. 10, 1995.
- Alomone Labs Candesartan cilexetil inhibits the activation of Angiotensin AT1R expressed in CHO-K1-mt Aequorin-Gα16 cells.Dose response curve for the inhibition of AT1R expressed in CHO-K1-mt aequorin-Gα16 cells. Ca2+ response, as detected by elevation in aequorin derived fluorescence following 0.04 nM Angiotensin II application, was inhibited by increasing concentrations of Candesartan cilexetil (#C-265). 10 nM Candesartan cilexetil fully inhibited the activation by Angiotensin II.
Angiotensin II is responsible for vasoconstriction in the renin-angiotensin system. In addition to its direct effect on blood vessels, it stimulates the synthesis and release of aldosterone and also promotes renal tubular reabsorption of sodium, resulting in water retention1.
Candesartan (Atacand, Parapres, Kenzen) is a synthetic antagonist of the Angiotensin II type 1 and 2 receptors. It has an effective concentration of 1-100 nM and an IC50 of 15 μg/kg. Candesartan is used for the treatment of essential hypertension and congestive heart failure with reduced ejection fraction under 40%. Moreover, Candesartan was found to be effective combined with hydrochlorodiazide for the treatment of severe hypertension. It is administered orally as a pro-drug which is activated by ester hydrolysis during absorption from the gut and has a low bioavailability of 15%. Candesartan has a higher affinity for the AT1 receptor than other drugs of its type such as irbesartan, valsartan and losartan, and also dissociates slower from the receptor enabling a longer half-life period of 9 hours. It is mainly secreted unchanged in the stool but undergoes some metabolism by CYP 2C92,3.