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Hey guys, in this video we will see angiotensin converting enzyme inhibitors we will cover relevant physiology, drugs, pharmacokinetic, side effects and drug interactions of ace inhibitors. as we have seen in video of renin angiotensin system, angiotensin converting enzyme is present on luminal side of vascular endothelium, this enzyme converts angiotensin i into angiotensin ii.
Another substrate for this enzyme is bradykinin, a vasodilator peptide. it mainly causes arteriolar constriction which increase peripheral resistance it also causes veno constriciton to some extend which increases venous return, causing increase in cardiac output which contributes in increasing blood pressure. apart from this, it also acts on adrenal cortex to increase
Aldosterone release. aldosterone acts on kidney and increases na and water retention. this increases blood volume which contributes in increasing blood pressure. another effect of aldosterone is increased k excretion. there is also an effect of angiotensin ii on renal vasculature this is renal corpuscle, this is its afferent arteriole and this is efferent arteriole.
Here angiotensin causes constriction of efferent arteriole. we will see the importance of this effect with relevant point later in the video. it increases synthesis of nitric oxide and prostacyclin. they cause vasodilatation which causes fall in blood pressure. drugs in this group are captopril, enalapril, enalaprilat, lisinopril, benazepril, fosinopril, trandolapril,
Quinapril, ramipril, moexipril and perindopril. and other drugs mostly follow profile of this drug. most of the drugs are given orally in form of tablets. however there few exceptions in this common features. captopril, enalaprilat and lisinopril are active by themselves. and fosinopril is eliminated by kidney as well as liver. this results in reduced synthesis of
Angiotensin ii and accumulation of bradykinin. we already know that angiotensin ii increases blood pressure in various ways. with ace inhibitors, there is no more angiotensin ii. so all these effects are lost, resulting in fall in blood pressure. also there is accumulation of bradykinin, which causes vasodilatation. this also contributes to some of the blood pressure
Lowering effect of ace inhibitors. the extend of antihypertensive effect depends on basal plasma renin activity initially, patients with high plasma renin activity shows more response. and patients with normal or low plasma renin activity shows less response. however in long term, all the patients show benefits, and ace inhibitors can be given regardless of plasma renin
Activity. reduced blood pressure by ace inhibitors reduces afterload on heart. this makes it easy for a failing heart to pump blood. ace inhibitors reduce mortality when used in post mi patients. in patients with high risk of cardiovascular events, where they are found to reduce risk of myocardial infarction, stroke and death. we have seen that angiotensin causes
Efferent arteriolar constriction now this pressure contributes to glomerular damage in diabetic nephropathy. so when you give ace inhibitors, there is no angiotensin so glomerular capillary pressure falls which reduces the damage. apart from this, ace inhibitors also increase the permeability selectivity of filtering membrane which contributes to beneficial effect in
Diabetic nephropathy. it is an emergency situation seen in patients with scleroderma. ace inhibitors play life saving role in this situation. it is seen at the initiation of therapy, especially in patients with you can start therapy with low dose rather than regular dose in such patients it is seen in patients with renal failure and those using potassium sparring diuretic.
We have seen that angiotensin causes release of aldosterone, which acts on kidney and increase potassium excretion. so now potassium, instead of being excreted, is reabsorbed, next 2 side effects are due to increased bradykinin level. its renal failure in patients with bilateral renal artery stenosis or stenosis in single remaining kidney and heart failure. see, enough
Glomerular filtration rate has to be maintained for kidney now one of the important determinant of gfr is glomerular capillary pressure. this pressure in tern depends on incoming pressure form afferent arteriole in normal individual, both these parameters are right enough however, in patients with renal artery stenosis or heart failure, there is reduced pressure at the
Afferent arteriole. luckily, angiotensin ii comes to rescue and balances the situation. it constricts efferent arteriole which helps maintain glomerular capillary pressure. now if you give ace inhibitors to such patients, our hero angiotensin ii is gone. so there is no balancing by efferent arteriole and glomerular capillary pressure falls. and it is better to avoid
These drugs during pregnancy. obviously, if you give potassium sparring diuretics on top of this, we know that vasodilator effect of bradykinin is mediated by nitric oxide so this vasodilator effect is lost if patient is taking nsaids simultaneously. angiotensin converting enzyme convers angiotensin i into angiotensin ii, angiotensin ii causes vasoconstriction, which
Increases blood pressure. it cases aldosterone release which cauuses na+ and water retention angiotensin also causes constriction of efferent arteriole in kidney. bradykinin causes synthesis of nitric oxide and prostacyclin they are given orally except enalaprilat which is given i.v. they are prodrugs, except captopril, enalaprilat and lisinopril which are active drugs.
They are mainly eliminated by kidney except fosinopril which is eliminated by kidney mechanism of action is inhibition of angiotensin converting enzyme resulting in reduced synthesis of angiotensin ii and accumulation of bradykinin. among uses are hypertension where benefits occur by reduced synthesis of angiotensin ii as well as vasodilatation by bradykinin. heart failure
Where decreased blood pressure decreases afterload and they are also useful in post mi patients and prophylactically in patients with in diabetic nephropathy, they reduces resistance at efferent arteriole which reduces intra-glomerularpressure which reduces glomerular damage. also they increase permeability selectivity of the filtering membrane. side effects include
Hypotension, hyperkalaemia due to reduced aldosterone level, dry cough and angioedema due to bradykinin accumulation. renal failure in patients with bilateral renal artery stenosis, stenosis in single remaining kidney and heart failure. drug interaction includes increased risk of hyperkalaemia in patients taking k+ sparring diuretics and loss of vasodilatation by bradykinin
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