The controversy over using ace inhibitors to treat hypertension
Arzoo Begum – N0361255
April 14th 2014
Abstract:
Renin is secreted as a proteolytic enzyme into the circulation that acts on the angiotensinogen released by the liver to be converted into angiotensin 1. This has no significant activity therefore it is converted via ACE to angiotensin 2. ACE converts up to 60% of angiotensin 1 to angiotensin 2. Angiotensin 2 interacts with subtype receptor AT1, which responds to cardiovascular effects, inflammation and vasoconstriction. The vasoconstriction causes a excretion of aldosterone by the adrenal gland. It also causes the retention of water and salt and helps excrete potassium in the kidneys, resulting in an increase of blood pressure. ACE inhibitors target ACE causing a reduction in angiotensin 2 and therefore decreasing aldosterone secretion and lowering blood pressure. Hypertension is known as a silent killer as the symptoms for it can sometimes go undetected, prolonged effects can lead to secondary conditions. ACE inhibitors prevent cardiovascular morbidity and mortality for patients that suffer from hypertension, left ventricle dysfunction and heart failure. ACE inhibitors can affect different patients differently, as in some they may work more effectively than others. The side effect profile of ACE inhibitors consists of a constant dry cough, weakness, fatigue and angioedema. This review paper aims to look into the controversy of ACE inhibitors and whether they should be encouraged to treat all types of hypertension. There are contradictions indicated on the reliability of ACE inhibitors being used as therapeutics towards hypertension. Nonetheless the research acquired highly recommends the use of ACE inhibitors, although they may bring about side effects
Key words: