The antihypertensive effectiveness and safety of dual RAAS blockade with aliskiren and valsartan.

The renin-angiotensin-aldosterone system (RAAS) is a major factor for the development and maintenance of hypertension and a major cause for cardiovascular remodeling and cardiovascular complications through its active peptide angiotensin (Ang) II. Blockade of RAAS with ACE inhibitors (ACEIs) results in suppression of Ang II levels, which eventually return to baseline levels after prolonged ACEI administration. This leads to an escape phenomenon through generation of Ang II from enzymes other than ACE and led to the hypothesis that dual blockade of RAAS with an ACEI/Ang receptor blocker (ARB) combination could lead to total blockade of RAAS, since ARBs block the action of Ang II at the AT1 receptor level, irrespective of the mechanism of Ang II generation and will have an additive blood pressure (BP)-lowering effect.

Proactive compared with passive adverse event recognition: calcium channel blocker-associated edema.

This article examines the concept of passive compared with proactive surveillance for monitoring adverse events occurring with antihypertensive medications, using the example of calcium channel blocker (CCB)-induced peripheral edema. Monitoring adverse events and clinical trial safety are important functions and dependent on investigator protocols and data and safety monitoring teams. Compared with proactive surveillance, voluntary reporting systems tend to yield a lower frequency of adverse events occurrence.

Pharmacological and clinical profile of moexipril: a concise review.

Angiotensin-converting enzyme (ACE) inhibitors are effective and safe antihypertensive drugs, with the exception of the rare occasion of angioedema. These drugs have demonstrated additional cardiovascular protective effects to their blood pressure lowering, and their combination with the diuretic hydrochlorothiazide potentiates their antihypertensive effectiveness. Moexipril is a long-acting ACE inhibitor suitable for once-daily administration, and like some ACE inhibitors, moexipril is a prodrug and needs to be hydrolyzed in the liver into its active carboxylic metabolite, moexiprilat, to become effective.