Relationship of lisinopril with kallikrein-kinin system in hypertensive patients in Erbil city, Iraq

* Directorate of Health, Erbil, Iraq. ** Department of Pharmacology and Toxicology, College of Pharmacy, Hawler Medical University, Erbil, Iraq. Introduction Hypertension (HTN) is characterized by a persistent progressive elevation in blood pressure. HTN is commonly defined as systolic blood pressure (SBP) ≥ 140 mmHg and diastolic blood pressure (DBP) ≥ 90 mmHg. It is typically asymptomatic state, with time it would disturb the renal, cardioand neuro-vascular system. HTN is etiologically classified into essential hypertension (EH) and secondary hypertension. EH is more common than secondary that affects 90-95 percent of persons who have HTN, resulting from the interaction between genetic and environmental factors. Secondary hypertension consists 5-10 percent of hypertensive patients with detectable and treatable causes that may results from deterioration in the hormonereliant endocrine system. Majority of trials emphasize on endothelial dysfunction (ED) in patients with EH as a result of reduction in nitric oxide (NO) synthesis owing to oxidative stress (OS). Impairment of NO and overproduction of angiotensin II (Ang II) will produce atherosclerosis through precipitating lipid and creation of fibrolipid Background and objective: Hypertension is characterized by a persistent, progressive elevation in blood pressure. Oxidative stress and endothelial dysfunction have a role in the pathogenesis of hypertension through interaction with the elements of the renin-angiotensin system. This study aimed to examine the effects of lisinopril on mean arterial pressure and biosubstances of Kallikrein-kinin-system (bradykinin), endothelial dysfunction (nitric oxide), and oxidative stress (malondialdehyde). Methods: A clinical trial was conducted in Erbil city from December 1, 2015 to August 10, 2016. The study included 65 patients with essential hypertension and 25 apparently healthy subjects; their ages were in between 18 and 55 years. The patients were receiving 10 mg lisinopril orally per day for six weeks as a starting dose. Results: At hypertension diagnosis, patients were with lower bradykinin and nitric oxide levels when compared with apparently healthy subjects; however, malondialdehyde level showed no significant difference when compared with of healthy subjects. After six weeks patients treatment, comparing bradykinin, nitric oxide, and malondialdehyde mean levels with their baselines, showed that significantly increased in bradykinin and nitric oxide (P <0.01) and significantly decreased in malondialdehyde (P <0.01). On the other hand, the differences between after treatment and healthy subjects had no significant difference, except bradykinin. Eventually, during treatment, the mean arterial pressure was significantly lowered. Conclusion: in addition to the significant lowering of blood pressure, lisinopril 10 mg daily for six weeks can significantly elevate kallikrein-kinin system and endothelial dysfunction markers, and significantly lowered in oxidative stress marker in hypertensive Kurd patients in Erbil city.