scholarly journals Role of the Renin-Angiotensin-Aldosterone System in Dystrophin-Deficient Cardiomyopathy

2020 ◽  
Author(s):  
Moises Rodriguez-Gonzalez ◽  
Manuel Lubian-Gutierrez ◽  
Helena Maria Cascales-Poyatos ◽  
Alvaro Antonio Perez-Reviriego ◽  
Ana Castellano-Martinez
Keyword(s):  
Therapeutic Strategy ◽  
Clinical Evidence ◽  
Enzyme Inhibitors ◽  
English Literature ◽  
Current Evidence ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Blockade ◽  
Comprehensive Search

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin-angiotensin-aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Also, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.

scholarly journals Role of the Renin–Angiotensin–Aldosterone System in Dystrophin-Deficient Cardiomyopathy

2020 ◽  
Vol 22 (1) ◽  
pp. 356
Author(s):  
Moises Rodriguez-Gonzalez ◽  
Manuel Lubian-Gutierrez ◽  
Helena Maria Cascales-Poyatos ◽  
Alvaro Antonio Perez-Reviriego ◽  
Ana Castellano-Martinez
Keyword(s):  
Therapeutic Strategy ◽  
Clinical Evidence ◽  
Enzyme Inhibitors ◽  
English Literature ◽  
Current Evidence ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Blockade ◽  
Comprehensive Search

Dystrophin-deficient cardiomyopathy (DDC) is currently the leading cause of death in patients with dystrophinopathies. Targeting myocardial fibrosis (MF) has become a major therapeutic goal in order to prevent the occurrence of DDC. We aimed to review and summarize the current evidence about the role of the renin–angiotensin–aldosterone system (RAAS) in the development and perpetuation of MF in DCC. We conducted a comprehensive search of peer-reviewed English literature on PubMed about this subject. We found increasing preclinical evidence from studies in animal models during the last 20 years pointing out a central role of RAAS in the development of MF in DDC. Local tissue RAAS acts directly mainly through its main fibrotic component angiotensin II (ANG2) and its transducer receptor (AT1R) and downstream TGF-b pathway. Additionally, it modulates the actions of most of the remaining pro-fibrotic factors involved in DDC. Despite limited clinical evidence, RAAS blockade constitutes the most studied, available and promising therapeutic strategy against MF and DDC. Conclusion: Based on the evidence reviewed, it would be recommendable to start RAAS blockade therapy through angiotensin converter enzyme inhibitors (ACEI) or AT1R blockers (ARBs) alone or in combination with mineralocorticoid receptor antagonists (MRa) at the youngest age after the diagnosis of dystrophinopathies, in order to delay the occurrence or slow the progression of MF, even before the detection of any cardiovascular alteration.

scholarly journals The Role of the Renin-Angiotensin-Aldosterone System in Cardiovascular Disease: Pathogenetic Insights and Clinical Implications

2021 ◽  
Author(s):  
Violeta Capric ◽  
Harshith Priyan Chandrakumar ◽  
Jessica Celenza-Salvatore ◽  
Amgad N. Makaryus
Keyword(s):  
Cardiovascular Disease ◽  
Renal Disease ◽  
Clinical Implications ◽  
Pathological Changes ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Blockade ◽  
Adverse Remodeling ◽  
Artery Disease

Increased attention has been placed on the activation of the renin-angiotensin-aldosterone system (RAAS) and pathogenetic mechanisms in cardiovascular disease. Multiple studies have presented data to suggest that cardiac and arterial stiffness leading to adverse remodeling of both the heart and vasculature leads to the various pathological changes seen in coronary artery disease, heart failure (with preserved and reduced ejection fractions), hypertension and renal disease. Over-activation of the RAAS is felt to contribute to these structural and endocrinological changes through its control of the Na+/K+ balance, fluid volume, and hemodynamic stability. Subsequently, along these lines, multiple large investigations have shown that RAAS blockade contributes to prevention of both cardiovascular and renal disease. We aim to highlight the known role of the activated RAAS and provide an updated description of the mechanisms by which activation of RAAS promotes and leads to the pathogenesis of cardiovascular disease.

scholarly journals Targeting the Renin–Angiotensin–Aldosterone System to Prevent Hypertension and Kidney Disease of Developmental Origins

2021 ◽  
Vol 22 (5) ◽  
pp. 2298
Author(s):  
Chien-Ning Hsu ◽  
You-Lin Tain
Keyword(s):  
Kidney Disease ◽  
Current Knowledge ◽  
Current Evidence ◽  
Developmental Origins ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Health And Disease ◽  
Nitric Oxide Deficiency ◽  
Developing Kidney ◽  
Prevention Of Hypertension

The renin-angiotensin-aldosterone system (RAAS) is implicated in hypertension and kidney disease. The developing kidney can be programmed by various early-life insults by so-called renal programming, resulting in hypertension and kidney disease in adulthood. This theory is known as developmental origins of health and disease (DOHaD). Conversely, early RAAS-based interventions could reverse program processes to prevent a disease from occurring by so-called reprogramming. In the current review, we mainly summarize (1) the current knowledge on the RAAS implicated in renal programming; (2) current evidence supporting the connections between the aberrant RAAS and other mechanisms behind renal programming, such as oxidative stress, nitric oxide deficiency, epigenetic regulation, and gut microbiota dysbiosis; and (3) an overview of how RAAS-based reprogramming interventions may prevent hypertension and kidney disease of developmental origins. To accelerate the transition of RAAS-based interventions for prevention of hypertension and kidney disease, an extended comprehension of the RAAS implicated in renal programming is needed, as well as a greater focus on further clinical translation.

scholarly journals Role of age, comorbidity and renin- angiotensin-aldosterone system in COVID-19. Effects of ACE inhibitors and angiotensin receptor blockers

Kardiologiia ◽  
2020 ◽  
Vol 60 (4) ◽  
pp. 4-9 ◽  
Author(s):  
Yu. V. Mareev ◽  
V. Yu. Mareev
Keyword(s):  
Enzyme Inhibitors ◽  
Angiotensin Receptor Blockers ◽  
Angiotensin Converting Enzyme Inhibitors ◽  
Converting Enzyme Inhibitors ◽  
Renin Angiotensin ◽  
Receptor Blockers ◽  
Relationship Of ◽  
The Relationship

The review addressed the relationship of coronavirus disease 2019 (COVID-19) with functioning of the renin-angiotensin-aldosterone axis and the causes for unfavorable prognosis depending on patients’ age and comorbidities. The authors discussed in detail potential effects of angiotensin-converting enzyme inhibitors and angiotensin II type 1 receptor antagonists on the risk of infection and the course of COVID-2019 as well as the effect of SARS-COV2 virus on the cardiovascular system.

scholarly journals Chronic vasodilation increases renal medullary PDE5A and α-ENaC through independent renin-angiotensin-aldosterone system pathways

2013 ◽  
Vol 305 (10) ◽  
pp. R1133-R1140 ◽  
Author(s):  
Crystal A. West ◽  
Stefan Shaw ◽  
Jennifer M. Sasser ◽  
Andrea Fekete ◽  
Tyler Alexander ◽  
...  
Keyword(s):  
Plasma Volume ◽  
Enzyme Inhibitor ◽  
Virgin Female ◽  
Normal Pregnancy ◽  
Female Rats ◽  
Plasma Volume Expansion ◽  
Renin Angiotensin Aldosterone System ◽  
Α Subunit ◽  
Renin Angiotensin

We have previously observed that many of the renal and hemodynamic adaptations seen in normal pregnancy can be induced in virgin female rats by chronic systemic vasodilation. Fourteen-day vasodilation with sodium nitrite or nifedipine (NIF) produced plasma volume expansion (PVE), hemodilution, and increased renal medullary phosphodiesterase 5A (PDE5A) protein. The present study examined the role of the renin-angiotensin-aldosterone system (RAAS) in this mechanism. Virgin females were treated for 14 days with NIF (10 mg·kg−1·day−1 via diet), NIF with spironolactone [SPR; mineralocorticoid receptor (MR) blocker, 200–300 mg·kg−1·day−1 via diet], NIF with losartan [LOS; angiotensin type 1 (AT1) receptor blocker, 20 mg·kg−1·day−1 via diet], enalapril (ENAL; angiotensin-converting enzyme inhibitor, 62.5 mg/l via water), or vehicle (CON). Mean arterial pressure (MAP) was reduced 7.4 ± 0.5% with NIF, 6.33 ± 0.5% with NIF + SPR, 13.3 ± 0.9% with NIF + LOS, and 12.0 ± 0.4% with ENAL vs. baseline MAP. Compared with CON (3.6 ± 0.3%), plasma volume factored for body weight was increased by NIF (5.2 ± 0.4%) treatment but not by NIF + SPR (4.3 ± 0.3%), NIF + LOS (3.6 ± 0.1%), or ENAL (4.0 ± 0.3%). NIF increased PDE5A protein abundance in the renal inner medulla, and SPR did not prevent this increase (188 ± 16 and 204 ± 22% of CON, respectively). NIF increased the α-subunit of the epithelial sodium channel (α-ENaC) protein in renal outer (365 ± 44%) and inner (526 ± 83%) medulla, and SPR prevented these changes. There was no change in either PDE5A or α-ENaC abundance vs. CON in rats treated with NIF + LOS or ENAL. These data indicate that the PVE and renal medullary adaptations in response to chronic vasodilation result from RAAS signaling, with increases in PDE5A mediated through AT1 receptor and α-ENaC through the MR.

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