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Renin Angiotensin Aldosterone System Blockers- A Review

Updated on February 10, 2012

This is a review of Renin Angiotensin Aldosterone blockers, including how they work, their therapeutic applications, their possible drug interactions and also their adverse effects. Please be aware that the information on this page has been written by me, and was originally part of a university project. Therefore, the use of this academic and commercial purposes is prohibited.

There are two main drug classes which block the Renin-Angiotensin-AldosteroneSystem (RAAS). These are Angiotensin Converting Enzyme Inhibitors and also Angiotensin-II antagonists. Renin inhibitors may also be used. These all work via the same overall pathway, but on different parts of the RAAS. In this pathway,Angiotensinogen is released from the liver which results in the conversion of Renin to Angiotensin-I. After this;ACE is released from the vascular endothelium which brings about the conversion of Angiotensin-I to Angiotensin-II.The end result of this is that there will be the secretion of aldosterone (this will cause an increase in salt and water reabsorption along with a reduction in potassium) which will increase blood pressure.It will also make the patient thirsty, which will prompt them to drink more and in turn again raising blood pressure(since the volume of water and therefore blood in the body has been increased). There will also be vasoconstriction again which will increase blood pressure.

Therefore, ACEI’s work by blocking ACE, which in turn will cause a reduction in Angiotensin-I being converted to Angiotensin-II,and reducing the level of it binding to its receptors as a whole. Angiotensin-II antagonists work on the same pathway.However,rather than preventing any conversion taking place, they bind to the Angiotensin-II receptor, therefore preventing Angiotensin-II from doing so,again resulting in a decreased response. Finally, Renin inhibitors can also be used to prevent the initial conversion of Angiotensinogen in the liver to Angiotensin-I, thereby prevent the activation of the RAAS pathway. However, these inhibitors are generally expensive and as a whole had a short half- life that there was little clinical benefit and they were also unable to betaken orally. The exception to this is Aliskiren.

Due to the effects of this pathway, it is clear to see that the therapeutic application of this is in those suffering from hypertension, with the intention to lower blood pressure. By doing so,it will reduce the risk of the patient suffering from CVD. The basis behind this is that hypertension is one of the biggest risk factors in CVD, with the other being dyslipidaemia.

With regard to ACEI’s such as Rampiril, there are numerous drug interactions. It is possible that it will cause hyperkalaemia when taking potassium salts, tacrolimus and also angiotensin- II antagonists. It can also result in hypoglycaemia in those that are also taking insulin and other antidiabetic agents. Furthermore,when taken in addition with NSAID’s such as diclofenac and ibuprofen, it can cause a reduction in its antihypertensive effect. ACEI’s as a whole also have numerous side effects. These include first dose hypotension, rash and angioneuroticoedema as well as cough.It can also cause a reduction in neutrophils (neutropaenia) and also changes in the sense of taste (Dysgeusia).

In the case of the Ang-II receptor antagonist Losartan, it too has numerous potential drug interactions and works not only in hypertension,but also in chronic heart failure. When tricyclic antidepressants are co-administered, it can result in an increase of its antihypertensive effect, resulting in hypotension. Much like in the case of Rampiril, when taken with potassium salts and also spironolactone it may result in an increase of potassium. Moreover, those suffering from manic depression and therefore on lithium have whilst on Losartan have beenfound to suffer from increased concentrations of lithium to the extent that it becomes toxic. However, this effect is reversible when the doses of each drug are adjusted. Also, when given with NSAID’s it can result in a decrease of renal function, to the extent that there is acute renal failure, especially in the elderly.Therefore,co-administration should be done with caution.It also has numerous side effects.These include common effects such as dizziness, fatigue,and also vertigo and uncommon effects such as palpitations, headaches and also abdominal pain in those with hypertension. In the case of chronic heart failure, the side effects are usually uncommon. There can be dyspnoea, dizziness, headache and also rash.

In the case of Aliskiren,it has been speculated that P-glycoprotein inducers such as rifampicin and StJohn’s Wort may decrease the bioavailability of Aliskiren. Moreover,for those on digoxin, its bioavailability maybe reduced by Aliskiren. Again, NSAID’s may bring about a reduction in its antihypertensive effects.Also, with the AUC and Cmax of Furosemide is reduced by 28 and 49%respectively.In terms of side effects,it has been found that these are relatively uncommon and rare.In some cases, there may be angioedema, a reduction in haemoglobin and also a raise in creatine levels.The patient may also suffer from diarrhoea.


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