Hyperkalemia is another common side effect. weeks or months later . The cough is predominantly seen in females and non-smokers [4,8C12]. However, the pathogenesis of ACE-I-induced cough remains controversial. The underlying mechanisms of the ACE-I-induced cough are multifactorial. Angiotensin-Converting Enzyme Inhibition Mechanism Angiotensin-converting enzyme (ACE) inhibition mechanism is a very important development in hypertension treatment. With ACE inhibition, the renin-angiotensin-aldosterone cascade is blocked. Generally, renin is produced and released in response to a decreased in blood flow to the juxtaglomerular apparatus of the kidney or in response to a decreased in the filtration of the sodium chloride concentration. It makes the degradation of hepatic angiotensinogen to its inactive peptide, angiotensin I. Then, angiotensin I is converted to active angiotensin II by BNC105 ACE produced by the capillaries in the alveoli. Angiotensin II has many physiological effects, such as increasing the resistance of blood vessels, causing adrenal cortex aldosterone release, and stimulating vasopressin [2,13C15]. ACE-I is a competitive inhibitor of ACE and prevents conversion of angiotensin I to angiotensin II. ACE is also responsible for the degradation of bradykinin. Active bradykinin is produced by its precursor kininogen, and kininogen is decomposed by kallikrein. Bradykinin has a short half-life because it is rapidly degraded by ACE (Figure 1) . Thus, the half-life of bradykinin can be prolonged by ACE-I with ACE inhibition, and its activity and concentration can increase. Angiotensin receptor blockers (ARBs), also known as angiotensin II receptor antagonists, cause vasodilatation, decrease vasopressin secretion, and decrease aldosterone production and secretion by blocking angiotensin II to bind to its receptors BNC105 . In ACE-I, ARBs are also indicated for hypertension, congestive heart failure (CHF), and diabetic nephropathy. They have no effect on ACE activities and do not cause inhibition of bradykinin degradation. Owing to this reason, some of the side effects of ACE-I and ARBs differ. Open in a separate window Figure 1 Effect of renin-angiotensin/kallikrein-kinin system on blood pressure regulation  ACE: angiotensin-converting enzyme; ADH: antidiuretic hormone; PG: prostaglandin Side Effects of ACE-I ACE-I t have some undesirable side effects. The side effects are often specific to the class of the medicine depending on its mechanism of action not the medicine itself. Owing to this reason, any ACE-I side effect can also occur with the use of other ACE-I. In a cohort study, 19% of patients using ACE-I have been shown to discontinue their medications due to side effects (mostly persisting cough) . Owing to its mechanism of action, hypotension due to ACE-I may occur and usually develop secondary to use with other medications that have a significant salt deprivation or diuretic effect . Hyperkalemia is another common side effect. The incidence of hyperkalemia in patients treated with ACE-I is approximately 3.3% [18,19]. Secondary cough and angioedema are idiosyncratic reactions to ACE-I, and these effects are dose-independent . In the cases of development of upper airway symptoms and cough with the use of this medicine in patients with obstructive Vegfa sleep apnea, disease severity may increase . In addition to the side effects due to the mechanism of action of ACE-I, specific side effects may occur depending on the drug molecular structure. For example, captopril sulfhydryl-related skin rash, neutropenia, tasting disorders, and nephritic BNC105 syndrome are some of its side effects. Some of these side effects are idiosyncratic, whereas.