The overexpression of tissue Angiotensin Converting Enzyme (ACE) has been shown to have adverse effects on the cardiovascular system. ACE is a zinc metalloprotease enzyme secreted by pulmonary and renal endothelial cells. Although ACE is mostly located on pulmonary endothelial cells, in the event of cardiovascular injuries or damage such as myocardial infarction and ischemic cardiomyopathy, it tends to concentrate in areas of injury and plays a major role in cardiac remodeling. Consequently, drugs that inhibit ACE have been used in the treatment of various cardiovascular diseases.
Angiotensin Converting Enzyme (ACE) acts as a catalyst in the conversion of angiotensin I to angiotensin II and plays an important role in the degradation of bradykinin. Angiotensin II is a very effective vasoconstrictor, while bradykinin is a strong vasodilator. Therefore, the overexpression of ACE leads to heart related diseases such as hypertension, myocardial infarction and heart failure. Angiotensin converting enzyme inhibitors block the conversion of angiotensin I to angiotensin II. Decreased levels of angiotensin II decrease plasma levels of aldosterone resulting in reduced sodium and water retention. This decreases blood pressure and enhances natriuresis. Contributing to these mechanisms, ACE inhibitors increase bradykinen levels, and, thus prostaglandin synthesis and further increase natriuresis. ACE inhibitors carry a cardio protective effect, possibly by substantially increasing the circulating natural stem cell regulator N-acetylseryl-aspartyl-lysyl-proline. Renin release will be increased related to blocked feedback loops of the renin angiotensin system. Thus, more angiotensin I is produced and, since it cannot be converted to angiotensin II when under pharmacological blockade, is ushereddown alternate metabolic pathways, resulting in increased production of vasodilator peptides.
Angiotensin converting enzyme inhibitors are also most effective for patient's whose hypertension is secondary to high renin production. When renin is released in excess, the renin angiotensin system is exaggerated resulting in increased circulating levels of angiotensin II, which exerts its vasoconstricting effects throughout the body. ACE inhibitors also may be prescribed to those in heart failure or with mitral regurgitation. These medications work specifically well for this population as left ventricular volume is reduced therefore decreasing both the workload of the heart and any regurgitant volume. ACE inhibitors have been shown to prevent or delay heart failure in patients with known systolic dysfunction. Therefore, ACE inhibitors are routinely prescribed to those with known disease or those who are at high risk for developing heart failure and systolic dysfunction. Because ACE inhibitors do not interfere with beta-receptor associated glucose regulation, they tend to be the safest choice for diabetic patients with hypertension, when compared to beta-blockers. ACE inhibitors also reduce the activation of low density lipoprotein receptors and therefore can reduce the risk of cardiovascular events.
ACE inhibitors such as lisinopril, fosinopril, enalapril, captopril, have been shown to exert beneficial cardiovascular effects including the maintenance of healthy blood pressure levels and in the alteration of cardiac remodeling after myocardial infarction.
Reference:Emily A. Buckley. Utilization of Vasopressin as a First Line Response to Perioperative Hypotension in the Patient on Angiotensin Receptor Antagonists and Angiotensin Converting Enzyme Inhibitors