ACE inhibitors, ARBs, Aliskiren

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Angiotensin-converting enzyme inhibitors (ACE inhibitors), along with closely associated agents such as angiotensin receptor blockers (ARBs) and aliskiren, are instrumental in mitigating the long-term progression of heart failure and enhancing patient survival. They exert their influence by inhibiting the renin-angiotensin-aldosterone system (RAAS), specifically curtailing the synthesis of aldosterone, a pivotal hormone for sodium and water resorption and the maintenance of blood pressure.

Renin, a protease discharged by the kidneys, commences this process. Renin catalyzes a sequence wherein angiotensinogen is transformed into angiotensin I. ACE is responsible for transforming angiotensin I into the the potent regulator angiotensin II. Angiotensin II plays a vital role in fluid and electrolyte balance, and in regulating arterial blood pressure. ACE inhibitors obstruct the transformation of angiotensin I to angiotensin II, negating the pressor actions of angiotensin II and facilitating natriuresis. ACE inhibitors are associated with several side effects, such as a dry cough due to increases bradykinins, hyperkalemia due to suppressed aldosterone production, and can precipitate pronounced hypotension in individuals with elevated renin. Other agents, such as ARBs and aliskiren, function in a parallel manner, targeting angiotensin II and renin respectively

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What is the primary function of ACE inhibitors and how do they work?

ACE inhibitors, identifiable by their "-pril" suffix, are medications primarily prescribed for hypertension and heart failure. They operate by inhibiting the angiotensin converting enzyme (ACE), which transforms angiotensin I into the potent vasoconstrictor, angiotensin II. By reducing angiotensin II production, ACE inhibitors diminish its effects on vasoconstriction and sodium retention, subsequently lowering blood pressure. Furthermore, they confer protective benefits in conditions like diabetic nephropathy and myocardial infarction by mitigating angiotensin II-induced cardiac remodeling.

What are potential adverse effects associated with the use of ACE inhibitors?

ACE inhibitors are typically well tolerated, but they aren't devoid of side effects. A notable adverse effect is a persistent dry cough, resulting from elevated bradykinin levels that irritate the lungs. Hyperkalemia can arise due to suppressed aldosterone production, and there might be a surge in angiotensin I and renin concentrations. In individuals with elevated renin, ACE inhibitors can precipitate pronounced hypotension and even syncope. Their teratogenic potential makes them contraindicated during pregnancy. Moreover, caution is advised when co-administered with NSAIDs or in patients with bilateral renal artery stenosis.

How do angiotensin receptor blockers (ARBs) compare to ACE inhibitors?

Angiotensin receptor blockers (ARBs), distinguished by their "-sartan" suffix, also serve to reduce blood pressure, akin to ACE inhibitors. However, rather than inhibiting angiotensin II production, ARBs block its receptors. This distinction often renders ARBs preferable for those intolerant to the dry cough associated with ACE inhibitors, given that ARBs don't elevate bradykinin levels. Nonetheless, much like ACE inhibitors, ARBs are associated with hyperkalemia due to reduced aldosterone secretion.

What is unique about aliskiren and how does it relate to ACE inhibitors and ARBs?

Aliskiren holds a distinct position as a direct renin inhibitor. Unlike ACE inhibitors and ARBs, which act downstream, aliskiren impedes renin's activity, directly inhibiting the conversion of angiotensinogen to angiotensin I. Similar to ACE inhibitors and ARBs, aliskiren can also elevate the risk of hyperkalemia due to a drop in aldosterone levels.

What effects do both ACE inhibitors and ARBs have on the GFR?

Both ACE inhibitors and ARBs can transiently reduce the glomerular filtration rate. This occurs because they dilate the efferent arterioles and lower the pressure gradient essential for filtration. Consequently, there might be a short-lived elevation in serum creatinine levels, a marker usually filtered by the kidneys. However, their enduring renal protective attributes, particularly in hypertension and diabetes, overshadow this initial decline in GFR.