Angiotensin-converting enzyme (ACE) inhibitors reduce the activity of the renin-angiotensin system (RAS).1-7 Inhibiting the ACE prevents the conversion of angiotensin I (Ang I) to angiotensin II (Ang II), reducing the circulating and local concentrations of Ang II. ACE inhibitors also reduce the amount of bradykinin broken down by ACEs, which leads to additional vasodilatation effects from increased bradykinin.4,5,8
The RAS regulates blood pressure and fluid electrolyte balance.9-14 Uncontrolled RAS leads to the development of hypertension and congestive heart failure. ACE catalyzes the conversion of Ang I to Ang II and inactivates bradykinin which is a vasodialator.7,14,15 Ang II is the primary hormone that mediates increased vasoconstriction, cardiac contractility, and cardiac, renal, and vascular hypertrophy, stimulates adrenal aldosterone secretion, and increases renal tubular sodium absorption.2,9,11,12,14,16 Increased aldosterone can increase reabsorption of sodium and the excretion of potassium by the kidney, which can result in increased salt and water retention, increased blood volume, and potassium loss.2,9-12,14,17 This combined with the vasoconstrictive effects of Ang II increases blood pressure.
References
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- Pimenta E, Gaddam KK, Pratt-Ubunama MN, et al. Aldosterone excess and resistance to 24-h blood pressure control. J Hypertens 2007; 25 (10): 2131-2137.