It is proven that angiotensin converting enzyme inhibitors is superior to receptor blockers. Is it the bradykinin accumulated by ACEI responsible for that? It causes the cough and limits the use of ACEI.
Angiotensin-I Converting Enzyme (ACE) is predominantly found in the pulmonary circulation (lungs) as well as vascular endothelilal of many tissues like adrenal cortex of the kidney, brain and heart. ACE converts the inactive decapeptide Angiotensin-I to vasoactive octapeptide Angiotensin-II. This same ACE also degrades or inactivates Bradykinin which is important for the synthesis of a vasodilator Nitric oxide (NO). Prolonged use of ACE Inhibitors like Captopril, Lisinopril, Ramipril etc leads to accumulation of Bradykinin thereby leading to more synthesis of NO which may have accounted for the cough. But from my own point of view ACEIs is not preferred or superior to Angiotensin Receptor Blockers (ARBs) because the later is not characterised with this cough side effect. Also, Medical Doctors prescribe ARBs (e.g Losartan) when the side effect of ACEIs is noticed. From our work, the use of nutraceuticals in managing hypertension is suggested to have very minimal or no side effects compared to synthetic drugs although this claim is yet to be clinically tested. I hope this information helps?
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