Efficacy of hemodialysis and the effects of certain displacing agents on plasma protein binding of sulfamethoxazole and sulfaphenazole in patients with chronic renal failure.

1980 ◽  
Vol 28 (1) ◽  
pp. 268-276 ◽  
Author(s):  
TAEKO KAWAMURA ◽  
NAOMI YAGI ◽  
HIROMI SUGAWARA ◽  
KAZUTAMA YAMAHATA ◽  
MASAHIKO TAKADA
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Protein Binding ◽  
Plasma Protein Binding ◽  
Plasma Protein

Plasma protein binding of frusemide in renal failure rabbits: investigation of endogenous protein binding inhibitors

1984 ◽  
Vol 36 (10) ◽  
pp. 663-667 ◽  
Author(s):  
KATSUMI IKEDA ◽  
HIRONORI YOSHITOMI ◽  
TAIJI NAKAYAMA ◽  
SHIGERU GOTO ◽  
TOSHIKIRO KIMURA
Keyword(s):  
Renal Failure ◽  
Protein Binding ◽  
Plasma Protein Binding ◽  
Plasma Protein ◽  
Endogenous Protein ◽  
Binding Inhibitors

Possible therapeutic interventions in COVID-19 induced ARDS by cotinine as an ACE-2 promoter and AT-1R blocker

2020 ◽  
Vol 20 ◽  
Author(s):  
Tarun Sharma ◽  
Sidharth Mehan
Keyword(s):  
Protein Binding ◽  
Plasma Protein Binding ◽  
Plasma Protein ◽  
Distress Syndrome ◽  
Therapeutic Interventions ◽  
Promising Candidate ◽  
Angiotensin Converting Enzyme 2 ◽  
Proinflammatory Effect ◽  
Pulmonary Permeability

: In these challenging times of the pandemic, as coronavirus disease 2019 (COVID-19) has taken over the planet, its complications such as acute respiratory distress syndrome (ARDS) have the potential to wipe out a large portion of our population. Whereas a serious lack of ventilators, vaccine being months away makes the condition even worse. That's why promising drug therapy is required. One of them was suggested in this article. It is the angiotensin-converting enzyme-2 (ACE-2) to which the COVID-19 virus binds and upon downregulation of which the pulmonary permeability increases and results in the filling of alveoli by proteinaceous fluids, which finally results in ARDS. ARDS can be assisted by angiotensinII type-1 receptor (AT-1R) blocker and ACE-2 upregulator. AT-1R blocker will prevent vasoconstriction, the proinflammatory effect seen otherwise upon its activation. ACE-2 upregulation will ensure less formation of angiotensin II, vasodilatory effects due to the formation of angiotensin (1-7), increased breakdown of bradykinin at lung level. Overall, decreased vasoconstriction of vessels supplying lungs and decreased vasodilation of lung tissues will ensure decreased pulmonary permeability and eventually relieve ARDS. It should also be considered that all components of the reninangiotensin-aldosterone system (RAAS) are located in the lung tissues. A drug with the least plasma protein binding is required to ensure its distribution across these lung tissues. Cotinine appears to be a promising candidate for COVID-19- induced ARDS. It acts across the board and acts as both an AT-1R blocker, ACE-2 upregulator. It also has a weak plasma protein binding that helps to spread through the lung tissues. In this review, we summarized that cotinine, along with COVID-19 virus replication blocker anti-virals, may prove to be a promising therapy for the treatment of COVID-19 induced ARDS.

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