Overview
- Jones, J.D. et al. (2011) P.T. 36, 634.
Alomone Labs Azilsartan inhibits the activation of AT1R expressed in CHO-K1-mt Aequorin-Gα16 cells.Dose-response curve for the inhibition of AT1R. Ca2+ response, as detected by elevation in aequorin derived fluorescence following 0.04 nM Angiotensin II application, was inhibited by increasing concentrations of Azilsartan (#A-245). 10 nM Azilsartan 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 retention.
Azilsartan is a synthetic antagonist of the angiotensin II receptor. It has an effective concentration of 1-100 nM and an IC50 of 2.6 nM on the human Angiotensin II type-1 receptor1. The antihypertensive effects of azilsartan are dose-related. A 32-mg dose of azilsartan decreases the maximal constrictive effect of Ang II by approximately 90% when the drug reaches peak plasma concentration.
The estimated bioavailability of azilsartan is 60% and it is not affected by food. Azilsartan is primarily metabolized by CYP 2C9. Its two main metabolites are M-1 and M-2. These metabolites have a low affinity towards the AT receptor and have no substantial pharmacological effect. Renal clearance of azilsartan is approximated to 2.3 ml/minute. Most of the product is eliminated in the feces (55%) and in urine (42%) while the rest remains unchanged.
Many clinical trials have shown a beneficial effect of azilsartan on the lowering of blood pressure. The most common side effect of azilsartan is diarrhea occurring in 2% of patients receiving 80-mg dose. Other possible adverse effects are nausea, muscle spasm, cough and dizziness2.
