Open AccessBradykinin as a Probable Aspect in SARS-Cov-2 Scenarios: Is Bradykinin Sneaking out of our Sight?
Author(s) -
Seyyed Mohammad Ghahestani,
Javad Mahmoudi,
Sakineh Hajebrahimi,
AmirBabak SioofyKhojine,
Hanieh SalehiPourmehr,
Fatemeh Sadeghi-Ghyassi,
Hadi Mostafaei
Publication year - 2020
Publication title -
iranian journal of allergy, asthma and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.357
H-Index - 25
eISSN - 1735-5249
pISSN - 1735-1502
DOI - 10.18502/ijaai.v19i(s1.r1).2850
Subject(s) - bradykinin , captopril , aprotinin , receptor , icatibant , medicine , pharmacology , angiotensin converting enzyme , virus , blockade , bradykinin receptor , immunology , blood pressure
The new virus SARS-CoV-2 is savagely spreading out over the world. The biologic studies show that the target receptor for the virus might be angiotensin-converting enzyme 2 (ACE2). This peptide is responsible for converting angiotensin II (Ang II), which is a profoundly active peptide, into Ang 1-7 with quite a balancing barbell function. It is emphasized that the direct target of the virus is ACE2 underlining the obvious difference with ACE. Nevertheless, we hypothesized that a back load build up effect on Ang II may usurp the ACE capacity and subsequently leave the bradykinin system unabated. We think there are clinical clues for dry cough and the presumed aggravating role of ACE inhibitors like captopril on the disease process. Thereby, we speculated that inhibition of bradykinin synthesis and/or blockade of bradykinin B2 receptor using Aprotinin/ecallantide and Icatibant, respectively, may hold therapeutic promise in severe cases and these molecules can be advanced to clinical trials.