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
- van Vark LC, Bertrand M, Akkerhuis KM, et al. Angiotensin-converting enzyme inhibitors reduce mortality in hypertension: a meta-analysis of randomized clinical trials of renin-angiotensin-aldosterone system inhibitors involving 158,998 patients. Eur Heart J 2012; 33 (16): 2088-2097.
- Te Riet L, van Esch JH, Roks AJ, van den Meiracker AH, Danser AH. Hypertension: renin-angiotensin-aldosterone system alterations. Circ Res 2015; 116 (6): 960-975.
- Taddei S, Virdis A, Ghiadoni L, Mattei P, Salvetti A. Effects of angiotensin converting enzyme inhibition on endothelium-dependent vasodilatation in essential hypertensive patients. J Hypertens 1998; 16 (4): 447-456.
- Izzo JL, Jr., Weir MR. Angiotensin-converting enzyme inhibitors. J Clin Hypertens (Greenwich) 2011; 13 (9): 667-675.
- Haefeli WE, Linder L, Luscher TF. Quinaprilat induces arterial vasodilation mediated by nitric oxide in humans. Hypertension 1997; 30 (4): 912-917.
- Atlas SA, Case DB, Sealey JE, Laragh JH, McKinstry DN. Interruption of the renin-angiotensin system in hypertensive patients by captopril induces sustained reduction in aldosterone secretion, potassium retention and natruiresis. Hypertension 1979; 1 (3): 274-280.
- Erdos EG. The angiotensin I converting enzyme. Fed Proc 1977; 36 (5): 1760-1765.
- Hornig B, Kohler C, Drexler H. Role of bradykinin in mediating vascular effects of angiotensin-converting enzyme inhibitors in humans. Circulation 1997; 95 (5): 1115-1118.
- Dzau VJ. Theodore Cooper Lecture: Tissue angiotensin and pathobiology of vascular disease: a unifying hypothesis. Hypertension 2001; 37 (4): 1047-1052.
- Guthrie GP, Jr. Angiotensin receptors: physiology and pharmacology. Clin Cardiol 1995; 18 (6 Suppl 3): Iii 29-34.
- Lemarie CA, Paradis P, Schiffrin EL. New insights on signaling cascades induced by cross-talk between angiotensin II and aldosterone. J Mol Med (Berl) 2008; 86 (6): 673-678.
- Mehta PK, Griendling KK. Angiotensin II cell signaling: physiological and pathological effects in the cardiovascular system. Am J Physiol Cell Physiol 2007; 292 (1): C82-97.
- Dzau VJ, Colucci WS, Hollenberg NK, Williams GH. Relation of the renin-angiotensin-aldosterone system to clinical state in congestive heart failure. Circulation 1981; 63 (3): 645-651.
- Reid IA. The renin-angiotensin system and body function. Arch Intern Med 1985; 145 (8): 1475-1479.
- Soffer RL. Angiotensin-converting enzyme and the regulation of vasoactive peptides. Annu Rev Biochem 1976; 45: 73-94.
- Sancho J, Re R, Burton J, Barger AC, Haber E. The role of the renin-angiotensin-aldosterone system in cardiovascular homeostasis in normal human subjects. Circulation 1976; 53 (3): 400-405.
- 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.
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