In this Review, we provide the latest insights into the complexity and interplay of the components of the non-canonical renin-angiotensin system, and discuss the function and therapeutic potential of targeting this system to treat cardiovascular disease.
As a counter-regulatory arm of the renin angiotensin system (RAS), the angiotensin-converting enzyme 2-angiotensin-(1-7)-MAS axis (ACE2-Ang-(1-7)-MAS axis) plays a protective role in cardiovascular diseases.
Current cardiovascular pharmacotherapy targets maladaptive overactivation of the renin-angiotensin-aldosterone system (RAAS), which occurs throughout the continuum of cardiovascular disease spanning from hypertension to heart failure with reduced ejection fraction.
Activation of renin-angiotensin- system, nitric oxide (NO•) bioavailability and subsequent sympathoexcitation plays a pivotal role in the pathogenesis of many cardiovascular diseases, including hypertension.
Previous studies indicate that perinatal compromise of taurine causes cardiovascular disorders in adults via the influence of taurine on renin-angiotensin system (RAS).
While the REN promoter is isolated from neighboring super-enhancers in most cells by insulators, these insulators break down with cell age to permit the inappropriate expression of REN in non-kidney cells by using the neighboring super-enhancers, resulting in expression in a wider spectrum of tissues, contributing to aging-related immune system dysregulation, cardiovascular diseases and cancers.
Presented herein, evidence in literature in support of a cross-talk between the renin-angiotensin system (RAS) and sympathetic nervous system (SNS), both known to be involved in the development of hypertension and cardiovascular disease, and as one of the underlying mechanisms of SUDEP.
The most frequent association observed among CVD preventive treatment was agents acting on the renin-angiotensin system and lipid-lowering drugs (5.1% of treated subjects).
Obesity may compound the increased risk of hypertension and cardiovascular disease in individuals born prematurely by further augmenting the prematurity-associated imbalance in the renin-angiotensin system.
Classic drugs, such as those targeting renin-angiotensin-aldosterone system, statins and aspirin remain first-line treatment options, both for primary and secondary prevention of CVD.
Despite the success of renin-angiotensin system (RAS) blockade by angiotensin-converting enzyme (ACE) inhibitors and angiotensin II type 1 receptor (AT<sub>1</sub>R) blockers, current therapies for hypertension and related cardiovascular diseases are still inadequate.
Previously, the inhibition of neurohormonal systems, namely the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, has proven to be useful in the treatment of many CVDs.
The exact mechanisms of how fetal programming events increase the risk of hypertension and cardiovascular disease are not fully elaborated; however, the focus on alterations in the biochemical components and functional aspects of the renin-angiotensin (Ang) system (RAS) has predominated, particularly activation of the Ang-converting enzyme (ACE)-Ang II-Ang type 1 receptor (AT<sub>1</sub>R) axis.
Recent Advances in the Knowledge of Naturally-derived Bioactive Compounds as Modulating Agents of the Renin-angiotensin-aldosterone System: Therapeutic Benefits in Cardiovascular Diseases.
We considered antihypertensive therapy and lipid-lowering therapy to be optimal when known patients with hypertension with albuminuria received renin-angiotensin system blockers and statins had been prescribed for overt cardiovascular disease.
The (pro)renin receptor (PRR) is an important member of the local tissue renin-angiotensin system and plays a vital role in many cardiovascular diseases.