Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate the role plasma kallikrein plays in the in vivo activation of inactive renin, we measured plasma active renin, inactive renin, kallikrein and prekallikrein levels in 10 patients with disseminated intravascular coagulation (DIC), with 16 normal persons as controls. The plasma active renin concentration was expressed by the angiotensin I generation rate after the addition of sheep renin substrate. Plasma inactive renin was activated by trypsin. The plasma total kallikrein level was measured by an assay of kallikrein activity on synthetic substrate S-2302 after the addition of a prekallikrein activator. Plasma kallikrein was assayed by its activity on S-2302 without addition of the activator. The prekallikrein level was obtained by subtracting the kallikrein activity from the total kallikrein activity. A significant decrease in the plasma prekallikrein concentration was observed in DIC patients, as compared to that of controls (p less than 0.01). There was no significant difference in plasma levels of kallikrein, inactive renin, and the proportion of active renin between DIC patients and normal controls, but the active renin level was higher in DIC patients. There was no significant correlation between the level of plasma kallikrein and the proportion of active renin in either normal controls or DIC patients. These results are compatible with, but do not prove, the theory that plasma kallikrein plays a role in the in vivo activation of inactive renin.
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PMID:Plasma active renin, inactive renin and kallikrein in patients with disseminated intravascular coagulation. 168 Sep 81

: ACE2 receptor has a broad expression pattern in the cellular membrane and provides a protective action against the development of cardiovascular diseases. Recently, this enzyme has become of extreme interest during the pandemic infection of COVID-19 (coronavirus disease 2019). This virus invades alveolar epithelium and cardiomyocytes using ACE2 as a transmembrane receptor. ACE2 is a counter-regulatory peptide that degrades Ang II into Ang 1-7, thereby attenuating the biological effects of the AT1 receptor. The binding between the spike protein of COVID-19 and the enzyme is crucial for the virus to enter the target cells, but whether an increase in ACE2 activity could facilitate the infection is not yet demonstrated. However, this aspect has raised many concerns about the use of ACE inhibitors or ARBs in infected patients or patients at risk of infection. It appears that cellular infection leads to a reduction in ACE2 expression and an increase in the activity of the Ang II--AT1 axis, which leads to the release of pro-inflammatory cytokines, ARDS, myocarditis, and hypercoagulability with the possibility of exacerbation of acute coronary syndrome, induction of pulmonary embolism, or appearance of disseminated intravascular coagulation. Therefore, ACE inhibitors or angiotensin receptor blocker drugs should be continued in infected patients, as their discontinuation can increase Ang II activity and induce injury to the lungs or cardiovascular system.
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PMID:Focus on clinical practice: angiotensin-converting enzyme 2 and corona virus disease 2019: pathophysiology and clinical implications. 3274 Apr 95