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Candesartan


Mechanism of action:

Candesartan is an angiotensin II receptor blocker that acts on the AT1 receptor, while its effect on the AT2 receptor is relatively limited. Angiotensin II is the main effector molecule of the renin-angiotensin-aldosterone system (RAAS). It normally acts through the AT1 receptor to cause vasoconstriction, thereby raising blood pressure, promote adrenal aldosterone secretion to increase sodium and water retention, stimulate the sympathetic nervous system, and promote vascular and myocardial hypertrophy. When candesartan competitively blocks the AT1 receptor, angiotensin II can no longer exert these effects, ultimately leading to vasodilation, reduced blood pressure, natriuresis and diuresis, and a reduction in the long-term adverse cardiovascular remodeling mediated by the AT1 receptor.

Reference(s):

1. Chen X et al. (2002). TTD: Therapeutic Target Database. Nucleic Acids Res. 


2. Cervenka L et al. (1999). Renal responses of the nonclipped kidney of two-kidney/one-clip Goldblatt hypertensive rats to type 1 angiotensin II receptor blockade with candesartan. J Am Soc Nephrol. 


3. Malmqvist K et al. (2000). Angiotensin II type 1 (AT1) receptor blockade in hypertensive women: benefits of candesartan cilexetil versus enalapril or hydrochlorothiazide. Am J Hypertens.

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