The renin-angiotensin-aldosterone system: focus on its distinct role in arterial hypertension and its various inhibitors as a therapeutic strategy to effectively lower blood pressure.

Chronically elevated blood pressure results from pathological alterations in control systems. Current approaches to elucidate the underlying etiology strongly emphasize the (patho)physiological significance of the Renin-Angiotensin-Aldosterone System (RAAS) which interestingly interacts with the sympathetic, the cholinergic and purinergic systems. While the angiotensin-II-receptor subtype 1 (AT1), which mediates the blood-pressure-related effects of angiotensin II (All), has so far been extensively investigated, the physiological relevance of the other angiotensin-II-receptor subtypes-in particular of the AT2-receptor subtype-is about to be evolved by analysis of the various signal transduction mechanisms and by evaluation of transgenic animals, e.g. the knock-out mice, following disruption of the single A-II-receptor subtypes. Based on the clinical success of ACE inhibitors, the blockade of the Renin-Angiotensin-Aldosterone System in many different ways has been recognized as a successful strategy to effectively lower blood pressure.