scholarly journals Anti-inflammatory drugs and the renin-angiotensin-aldosterone system: Current knowledge and potential effects on early SARS-CoV-2 infection

2021 ◽  
Vol 291 ◽  
pp. 198190
Author(s):  
Iris Louise N. Cabbab ◽  
Rafael Vincent M. Manalo
Keyword(s):  
Current Knowledge ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

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 Renin-angiotensin-aldosterone system inhibitors – a realm of confusion in COVID-19

2021 ◽  
Vol 4 (Special2) ◽  
pp. 389-394
Author(s):  
Angela Madalina Lazar
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Current Knowledge ◽  
Angiotensin Receptor Blockers ◽  
Protective Effects ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Inhibitors

Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 patients. Worldwide, millions of patients receive RAAS inhibitors for the treatment of hypertension and other important comorbidities. In this context, knowledge of the exact effect of these medications becomes of crucial significance. This paper aims to fill in a gap in the current knowledge and presents a putative mechanism by which RAAS inhibitor administration's beneficial results can be explained better. RAAS inhibitors can be beneficial, as they counteract the excessive detrimental activation of the classical angiotensin-converting enzyme (ACE) axis, decreasing the angiotensin II levels. The angiotensin receptor blockers (ARBs) increase the angiotensin II levels, while the angiotensin-converting enzyme inhibitors (ACEI) increase the angiotensin I levels; these substrates will compete with the SARS-CoV-2 for the ACE2 binding, decreasing the viral infectivity. In addition, following the RAAS inhibitors treatment, the up-regulated ACE2 will cleave these substrates (angiotensin I and II), particularly to angiotensin 1-7 that possesses vasodilator, protective effects.

scholarly journals Active Anti-Inflammatory and Hypolipidemic Derivatives of Lorazepam

Molecules ◽  
2019 ◽  
Vol 24 (18) ◽  
pp. 3277
Author(s):  
Panagiotis Theodosis-Nobelos ◽  
Georgios Papagiouvannis ◽  
Panos N. Kourounakis ◽  
Eleni A. Rekka
Keyword(s):  
Acute Inflammation ◽  
Current Knowledge ◽  
Rat Plasma ◽  
Straightforward Method ◽  
Inflammatory Drugs ◽  
Multifunctional Agents ◽  
Anti Inflammatory ◽  
High Yields ◽  
Derivatives Of ◽  
And Oxidative Stress

Novel derivatives of some non steroidal anti-inflammatory drugs, as well as of the antioxidants α-lipoic acid, trolox and (E)-3-(3,5-di-tert-butyl-4-hydroxyphenyl)acrylic acid with lorazepam were synthesised by a straightforward method at satisfactory to high yields (40%–93%). All the tested derivatives strongly decreased lipidemic indices in rat plasma after Triton induced hyperlipidaemia. They also reduced acute inflammation and a number of them demonstrated lipoxygenase inhibitory activity. Those compounds acquiring antioxidant moiety were inhibitors of lipid peroxidation and radical scavengers. Therefore, the synthesised compounds may add to the current knowledge about multifunctional agents acting against various disorders implicating inflammation, dyslipidaemia and oxidative stress.

scholarly journals The role of the angiotensins in the pathogenesis of inflammatory joint disease

2021 ◽  
Vol 93 (5) ◽  
pp. 635-639
Author(s):  
Andrei V. Gordeev ◽  
Elena A. Galushko ◽  
Natalia M. Savushkina
Keyword(s):  
Cardiovascular System ◽  
The Body ◽  
Joint Disease ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
In Vivo Experiments ◽  
Anti Inflammatory

The significant humoral effect of the renin-angiotensin-aldosterone system on the regulation of the cardiovascular system and blood pressure has long been widely known. However, the identification and interpretation of new components of renin-angiotensin-aldosterone system in recent years can significantly expand the range of its potential effects on the body. The anti-inflammatory effect of drugs that block angiotensin II and its receptors, including in rheumatic diseases, can become practically significant for General therapists by their effect on reducing the concentration of inflammatory mediators and angiogenesis processes. The organoprotective and anti-inflammatory potentials of drugs that reduce the production of at demonstrated in vitro and in vivo experiments allow us to consider them as first-line angiotropic agents in patients with rheumatoid arthritis, especially in the presence of pathology of the cardiovascular system and kidneys.

Electrolyte transport in the renal collecting duct and its regulation by the renin–angiotensin–aldosterone system

2019 ◽  
Vol 133 (1) ◽  
pp. 75-82
Author(s):  
Osamu Yamazaki ◽  
Kenichi Ishizawa ◽  
Daigoro Hirohama ◽  
Toshiro Fujita ◽  
Shigeru Shibata
Keyword(s):  
Current Knowledge ◽  
Collecting Duct ◽  
Salt Transport ◽  
Electrolyte Transport ◽  
Intercalated Cells ◽  
Transport Mechanisms ◽  
Cortical Collecting Duct ◽  
Distal Nephron ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin

Abstract Distal nephron of the kidney plays key roles in fluid volume and electrolyte homeostasis by tightly regulating reabsorption and excretion of Na+, K+, and Cl−. Studies to date demonstrate the detailed electrolyte transport mechanisms in principal cells of the cortical collecting duct, and their regulation by renin–angiotensin–aldosterone system (RAAS). In recent years, however, accumulating data indicate that intercalated cells, another cell type that is present in the cortical collecting duct, also play active roles in the regulation of blood pressure. Notably, pendrin in β-intercalated cells not only controls acid/base homeostasis, but is also one of the key components controlling salt and K+ transport in distal nephron. We have recently shown that pendrin is regulated by the co-ordinated action of angiotensin II (AngII) and aldosterone, and at the downstream of AngII, mammalian target of rapamycin (mTOR) signaling regulates pendrin through inhibiting the kinase unc51-like-kinase 1 and promoting dephosphorylation of mineralocorticoid receptor (MR). In this review, we summarize recent advances in the current knowledge on the salt transport mechanisms in the cortical collecting duct, and their regulation by the RAAS.

Oxidative stress and inflammation in the evolution of heart failure: From pathophysiology to therapeutic strategies

2019 ◽  
Vol 27 (5) ◽  
pp. 494-510 ◽  
Author(s):  
Alberto Aimo ◽  
Vincenzo Castiglione ◽  
Chiara Borrelli ◽  
Luigi F Saccaro ◽  
Maria Franzini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Current Knowledge ◽  
Interleukin 1 ◽  
Prognostic Significance ◽  
Deep Understanding ◽  
Future Research ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Both oxidative stress and inflammation are enhanced in chronic heart failure. Dysfunction of cardiac mitochondria is a hallmark of heart failure and a leading cause of oxidative stress, which in turn exerts detrimental effects on cellular components, including mitochondria themselves, thus generating a vicious circle. Oxidative stress also causes myocardial tissue damage and inflammation, contributing to heart failure progression. Furthermore, a subclinical inflammatory state may be caused by heart failure comorbidities such as obesity, diabetes mellitus or sleep apnoeas. Some markers of both oxidative stress and inflammation are enhanced in chronic heart failure and hold prognostic significance. For all these reasons, antioxidants or anti-inflammatory drugs may represent interesting additional therapies for subjects either at high risk or with established heart failure. Nonetheless, only a few clinical trials on antioxidants have been carried out so far, with several disappointing results except for vitamin C, elamipretide and coenzyme Q10. With regard to anti-inflammatory drugs, only preliminary data on the interleukin-1 antagonist anakinra are currently available. Therefore, a comprehensive, deep understanding of our current knowledge on oxidative stress and inflammation in chronic heart failure is key to providing some suggestions for future research on this topic.

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