ACE was found by Skeggs and colleagues, they reported in 1954–1956 that renin liberates a decapeptide Ang I, which is converted by a factor in horse plasma, to the active peptide to Ang II in presence of Cl−. They named this factor angiotensin converting enzyme(ACE). As we all know ACE inhibitors are important drugs with great benefit to our patients[1]
Which disease is treated by ACE inhibitors.
Early researcher Rochon.demonstrates improvement in clinical outcomes in elderly patients with heart failure who were treated with ACE inhibitors.This study reinforces and extends the known benefit of ACE inhibitors for congestive heart failure. The study’s conclusion of a causal relationship between the use of ACE inhibitors and improved outcome is strengthened by the dose-response relationship
low-dose treatment with ACE inhibitors can benefit prevent or delay diabetic nephropathy. The inclusion of ACE inhibitor therapy is an element of a combined aggressive approach shown to be effective in significantly reducing cardiovascular mortality and nephropathy in type 2 diabetes
Independent of their blood pressure lowering effect, ACE inhibitors are thought to reduce vascular inflammation[2]
Side effects induced by ACE inhibitors.
One side effects is ACE inhibitor-induced cough. The outcome of Morimoto research gives relative weights to various known associations with ACE inhibitor-induced cough, and help predict the likelihood that this adverse event will occur or recur if an ACE inhibitor is administered to a patient. with the possible exception of those who have previously developed ACE inhibitor-induced cough. The angiotensin receptor blockers (ARBs) are reasonable alternatives for patients who do develop ACE inhibitor-induced cough. Another side effects is coused by ACE inhibitors is mild renal dysfunction as the desired result of reducing intraglomerular pressure, thereby preventing damage if hypertension coexists with diabetes. A slight rise in serum creatinine is to be expected and is acceptable after starting an ACE inhibitor. If the serum creatinine rises more than 30% above baseline or progressively increases over time, the clinician should promptly discontinue the ACE inhibitor and consider renovascular disease or other conditions known to enhance ACE inhibitor nephrotoxicity. The recent research demonsted that more evidence that antihypertensive agents, particularly centrally acting ACE inhibitors (CACE-Is), which cross the blood-brain barrier, are associated with a reduced rate of cognitive decline[3]. The side effect perhaps caused by incorrect or insufficient dosing of ACE inhibitors. these agents are used for three different indications, and the therapeutic approach for each indication is different. In order to improve the delivery of this important treatment to our patients with diabetes, hypertension, or congestive heart failure, the clinical leadership in academic medical centers and affiliated sites, need to be role models in the proper use of these medications and tireless in teaching these concepts[4].
[1] Ervin G. Erdös, The ACE and I: how ACE inhibitors came to be. The FASEB Journal. 2006, 20(8),1034-1038 [2] Kortekaas KE, Meijer CA, Hinnen JW.ea al, ACE inhibitors potently reduce vascular inflammation, results of an open proof-of-concept study in the abdominal aortic aneurysm.PLoS One. 2014, 9(12) e111952 [3 ]Gao Y, O’Caoimh R, Healy L, et al, Effects of centrally acting ACE inhibitors on the rate of cognitive decline in dementia. Kerins DM. BMJ Open. 2013 Jul 25;3(7) e002881 [4] Brent G Petty, The Place for ACE Inhibitors.J Gen Intern Med. 2004, 19(6): 710–711.
