ACE inhibitors share a "-pril" suffix, and include drugs like captopril, enalapril, and lisinopril.
These drugs were initially developed to treat hypertension, and can be used alone or in combination. It was later that they were found to be helpful in other renal and cardiovascular diseases.
ACE inhibitors are indicated to treat CHF, when left ventricular systolic dysfunction exists. They can also be used in angina, cardiac ischemia, and post-MI patients.
ACE inhibitors are effective in treating diabetic nephropathy, caused by diabetes mellitus. Research has shown that ACE inhibitors are renal protective and slow the associated morphological changes in the glomeruli seen with renal disease.
ACE inhibitors inhibit angiotensin-converting enzyme, which is secreted by the lungs and kidneys. This inhibition prevents the formation of angiotensin II, thus preventing activation of AT-1 receptors in the adrenal cortex. Furthermore, this leads to lowered aldosterone levels.
Angiotensin II maintains or even increases glomerular filtration rate (GFR) by preferentially constricting the efferent arteriole. ACE inhibitors prevent the formation of Angiotensin II. This causes relaxation of the efferent arteriole so GFR decreases. For this reason, ACE inhibitors are contraindicated in patients with bilateral renal artery stenosis as these patients already have a low GFR from low RBF.
ACE inhibitors block efferent arteriolar constriction (normally caused by angiotensin II), thus decreasing GFR. It should be noted that there will be increased concentration of renin because of the negative feedback of angiotensin I to angiotensin II conversion.
Inhibition of angiotensin converting enzyme leads to increased levels of bradykinin, which is a potent vasodilator and is associated with a dry cough.
A common adverse effect of ACE inhibitors is a persistent dry cough, often associated with the increases in the levels of bradykinin.
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