Aliskiren is the first drug in a new class of antihypertensives: the renin inhibitors. Aliskiren selectively inhibits the first enzymatic conversion in the cascade of the renin-angiotensin-aldosterone system (RAAS). This selective inhibition prohibits the formation of angiotensin I from angiotensinogen by the enzyme renin. This action of aliskiren inhibits the production of angiotensin II and aldosterone. Decrease of angiotensin II and aldosterone concentrations results in direct vasodilation, decreased sympathetic activity, and increased excretion of water and sodium by the kidneys. Deactivation of the RAAS, including all the events mentioned above, ultimately leads to a decrease in systolic and diastolic blood pressures. All agents that block the RAAS (ACE inhibitors, AII antagonists, aldosterone antagonists) inhibit the negative feedback loop, leading to a compensatory rise
in renin concentration. Aliskiren is special because it inhibits the RAAS at its origin. Furthermore and in contrast to other RAAS-blocking agents, aliskiren decreases the plasma renin activity despite the compensatory rise in renin concentration. Another distinguishing feature of aliskiren is that it does not interfere with other metabolic pathways such as the degradation of bradykinin. This might, however, result in a lower antihypertensive effect; on the other hand, this characteristic reduces the incidence of adverse effects in comparison with other RAAS-blocking agents. Aliskiren is only registered for the treatment of essential hypertension and is currently not widely applied in clinical practice. Diarrhoea is the most common adverse effect, followed by cough. Peripheral oedema, rash, and influenza may also occur among patients treated with aliskiren.
EPAR of aliskiren