The renin–angiotensin–aldosterone system (RAAS) regulates the body’s haemodynamic equilibrium, circulating volume, and electrolyte balance, and is a key therapeutic target in hypertension, the world’s leading cause of premature mortality [1]. Hypertensive disorders are strongly linked with an overactive RAAS [2], and RAAS inhibitors such as angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are routinely used to treat high blood pressure (BP) [3]. BP reduction is one of the main goals of current European hypertension guidelines [4]. Oral ACE inhibitors, the oldest category of RAAS inhibitor, were commercially released in the early 1980s, more than a decade before the first ARBs became available [5]. The introduction of ACE inhibitors heralded major changes in the way hypertension and cardiovascular (CV) disease were treated. Although the decision of the medical community to replace older ACE inhibitors with more modern ARBs in the 1990s was debatable, it did nevertheless allow scientists to learn more about the angiotensin receptors involved in RAAS stimulation. This and much else of value have been discovered since RAAS inhibitors first became available, but some surprising gaps in our knowledge still exist. Until recently, the effect of RAAS inhibition on mortality in hypertension was unknown. This question was recently addressed by a meta-analysis of randomised controlled trials in populations who received contemporary antihypertensive medication [6]. The results of this meta-analysis have helped elucidate the long-term consequences of treatment with RAAS inhibitors on mortality in hypertension. This article will consider the differences between RAAS inhibitors in terms of their pharmacological and clinical effects, and analyse the impact of the main types of RAAS inhibitor, ACE inhibitors and ARBs, on mortality reduction in hypertensive patients with reference to this latest metaanalysis

RAAS inhibition and mortality in hypertension: from pharmacology to clinical evidence

FERRARI, Roberto
2013

Abstract

The renin–angiotensin–aldosterone system (RAAS) regulates the body’s haemodynamic equilibrium, circulating volume, and electrolyte balance, and is a key therapeutic target in hypertension, the world’s leading cause of premature mortality [1]. Hypertensive disorders are strongly linked with an overactive RAAS [2], and RAAS inhibitors such as angiotensinconverting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) are routinely used to treat high blood pressure (BP) [3]. BP reduction is one of the main goals of current European hypertension guidelines [4]. Oral ACE inhibitors, the oldest category of RAAS inhibitor, were commercially released in the early 1980s, more than a decade before the first ARBs became available [5]. The introduction of ACE inhibitors heralded major changes in the way hypertension and cardiovascular (CV) disease were treated. Although the decision of the medical community to replace older ACE inhibitors with more modern ARBs in the 1990s was debatable, it did nevertheless allow scientists to learn more about the angiotensin receptors involved in RAAS stimulation. This and much else of value have been discovered since RAAS inhibitors first became available, but some surprising gaps in our knowledge still exist. Until recently, the effect of RAAS inhibition on mortality in hypertension was unknown. This question was recently addressed by a meta-analysis of randomised controlled trials in populations who received contemporary antihypertensive medication [6]. The results of this meta-analysis have helped elucidate the long-term consequences of treatment with RAAS inhibitors on mortality in hypertension. This article will consider the differences between RAAS inhibitors in terms of their pharmacological and clinical effects, and analyse the impact of the main types of RAAS inhibitor, ACE inhibitors and ARBs, on mortality reduction in hypertensive patients with reference to this latest metaanalysis
Ferrari, Roberto
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1951212
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