scholarly journals Lock, Stock and Barrel: Role of Renin-Angiotensin-Aldosterone System in Coronavirus Disease 2019

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1752
Author(s):  
Christian Zanza ◽  
Michele Fidel Tassi ◽  
Tatsiana Romenskaya ◽  
Fabio Piccolella ◽  
Ludovico Abenavoli ◽  
...  
Keyword(s):  
Cell Receptor ◽  
Normal Function ◽  
Host Cells ◽  
Viral Agent ◽  
Exact Role ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Inflammatory State ◽  
The Subject

Since the end of 2019, the medical-scientific community has been facing a terrible pandemic caused by a new airborne viral agent known as SARS-CoV2. Already in the early stages of the pandemic, following the discovery that the virus uses the ACE2 cell receptor as a molecular target to infect the cells of our body, it was hypothesized that the renin-angiotensin-aldosterone system was involved in the pathogenesis of the disease. Since then, numerous studies have been published on the subject, but the exact role of the renin-angiotensin-aldosterone system in the pathogenesis of COVID19 is still a matter of debate. RAAS represents an important protagonist in the pathogenesis of COVID19, providing the virus with the receptor of entry into host cells and determining its organotropism. Furthermore, following infection, the virus is able to cause an increase in plasma ACE2 activity, compromising the normal function of the RAAS. This dysfunction could contribute to the establishment of the thrombo-inflammatory state characteristic of severe forms of COVID19. Drugs targeting RAAS represent promising therapeutic options for COVID19 sufferers.

scholarly journals Role of MicroRNAs in Renin-Angiotensin-Aldosterone System-Mediated Cardiovascular Inflammation and Remodeling

2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Maricica Pacurari ◽  
Paul B. Tchounwou
Keyword(s):  
Gene Expression ◽  
Cardiovascular Disease ◽  
Early Stage ◽  
Inflammatory Factors ◽  
Therapeutic Approaches ◽  
Exact Role ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Endogenous Regulators

MicroRNAs are endogenous regulators of gene expression either by inhibiting translation or protein degradation. Recent studies indicate that microRNAs play a role in cardiovascular disease and renin-angiotensin-aldosterone system- (RAAS-) mediated cardiovascular inflammation, either as mediators or being targeted by RAAS pharmacological inhibitors. The exact role(s) of microRNAs in RAAS-mediated cardiovascular inflammation and remodeling is/are still in early stage of investigation. However, few microRNAs have been shown to play a role in RAAS signaling, particularly miR-155, miR-146a/b, miR-132/122, and miR-483-3p. Identification of specific microRNAs and their targets and elucidating microRNA-regulated mechanisms associated RAS-mediated cardiovascular inflammation and remodeling might lead to the development of novel pharmacological strategies to target RAAS-mediated vascular pathologies. This paper reviews microRNAs role in inflammatory factors mediating cardiovascular inflammation and RAAS genes and the effect of RAAS pharmacological inhibition on microRNAs and the resolution of RAAS-mediated cardiovascular inflammation and remodeling. Also, this paper discusses the advances on microRNAs-based therapeutic approaches that may be important in targeting RAAS signaling.

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.

Role of the Renin-Angiotensin-Aldosterone System in the Regulation of Plasma Potassium in Chronic Renal Disease

Nephron ◽  
1975 ◽  
Vol 15 (1) ◽  
pp. 35-49 ◽  
Author(s):  
P. Weidmann ◽  
M.H. Maxwell ◽  
P. Rowe ◽  
R. Winer ◽  
S.G. Massry
Keyword(s):  
Renal Disease ◽  
Chronic Renal Disease ◽  
Plasma Potassium ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

scholarly journals Uterine fibroids and risk of hypertension: Implication of inflammation and a possible role of the renin-angiotensin-aldosterone system

2018 ◽  
Vol 20 (4) ◽  
pp. 727-729 ◽  
Author(s):  
Decio Armanini ◽  
Chiara Sabbadin ◽  
Gabriella Donà ◽  
Luciana Bordin ◽  
Loris Marin ◽  
...  
Keyword(s):  
Uterine Fibroids ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

Role of the renin-angiotensin-aldosterone system in hypertensive children with coarctation of the aorta

1979 ◽  
Vol 43 (4) ◽  
pp. 828-834 ◽  
Author(s):  
Bruce S Alpert ◽  
Hugh H Bain ◽  
J.Williamson Balfe ◽  
B.S.Langford Kidd ◽  
Peter M Olley
Keyword(s):  
Coarctation Of The Aorta ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin
Sign in / Sign up

Export Citation Format

Share Document