High altitude pulmonary edema (HAPE) remains the major cause of death related to high altitude exposure with a high mortality in absence of emergency treatment. Due to the deprival of oxygen in higher altitudes, the blood vessels constricts and squeezes blood in the vessels. This makes pressure to go up which in turn forces blood into air pockets in lungs that can kill people with HAPE. Angiotensin Converting Enzyme (ACE) is found in lung capillaries. It catalyses conversion of angiotensin I to angiotensin II which is a potent vasoconstrictor and inactivates bradykinin which is a potent vasodilator thereby causing HAPE. Tripeptides Val-Pro-Pro (VPP) and Ile-Pro-Pro (IPP) act as ACE inhibitors, that reduce vasoconstriction and facilitate vasodilation, so that they can be used in the treatment of HAPE. Enzyme-inhibitor docking is performed between Angiotensin I Converting Enzyme ACE and two natural inhibitors, tripeptides Val-Pro-Pro (VPP) and Ile-Pro-Pro (IPP) using the Patchdock Software. The docking study provided a quantitative energetic measure (Atomic Contact Energy) of 262.56 and 147.73 for ACE inhibition by VPP and IPP respectively. This ensures that the tripeptides Val-Pro-Pro (VPP) and Ile-Pro-Pro (IPP) are able to inhibit the activity of the ACE which in turn can induce decreased formation of Angiotensin II and decreased inactivation of bradykinin thereby it can alleviate HAPE.
Key words: High altitude pulmonary edema (HAPE), angiotensin converting enzyme, Val-Pro-Pro, Ile-Pro-Pro, patchdock
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