Background & Objective: As renin-angiotensin system (RAS) activity could affect the severity of oxidative stress and inflammatory markers the effect of enalapril and losartan on these markers in renal transplant recipients (RTRs) with RAS polymorphisms was assessed.

 Methods: After determination of RAS genotypes including angiotensin converting enzyme (ACE I/D), Angiotensinogen (AGT M235T) and angiotensin II type 1 receptor (ATR1 A1166C) by PCR, seventy-six RTRs recruited to four groups randomly: first group (17 patients) and second group (24 patients) were treated with E (E⁺: 10mg/daily) and L (L⁺: 50 mg/daily) alone, respectively. The third group (17 patients as positive control) received E+L (E⁺L⁺: 10mg/daily + 50 mg/daily) and the 4^th group (18 patients as negative control) received no medication (E^-L^-). Hs-CRP and total anti-oxidant (TA) as inflammatory and anti-oxidative markers were measured after 2 months. After 2 weeks as washout period, E group changed to L and vice versa as a cross-over design. They were followed for another 8 weeks and hs-CRP and TA were retested.

 Results: Following up the patients (after 2, 4 months of treatment) in treated groups revealed that hs-CRP and TA levels were significantly decreased and increased (consequently) in E⁺L⁺, L⁺, E⁺ groups (P<0.05). On analyzing the relationship between RAS polymorphisms with baseline hs-CRP and TA levels, CC genotype of ATR1 had lower hs-CRP levels (P=0.04). But none of the RAS polymorphisms could predict the anti-oxidative and anti-inflammatory response rate to the drugs (P>0.05).

 Conclusion: E and/or L reduce hs-CRP and increase TA regardless of the RAS genotypes.

 Background & objectives: Ischemic brain edema is one of the most important complications of cerebral infarction. Edema aggravates the primary ischemic injury to the brain. It was demonstrated that the renin-angiotensin system (RAS) and its active peptide angiotensin II involved in ischemic brain injury. But role of RAS in the formation of ischemic edema is not clear. The present study was conducted to investigate the effects of the RAS inhibition by enalapril on edema formation and blood-brain barrier (BBB) disruption.

 Methods: In this research frothy Sprague Dawley male rat in six groups were studied. Animals were anesthetized with chloral hydrate (400mg/kg, IP). Transient focal cerebral ischemia was induced by occlusion of right middle cerebral artery using intraluminal filament method. Three groups of animals as sham, ischemic and enalapril receiving (0.03mg/kg) groups were studied for assessment of neurological outcome and brain edema formation. 24 hours following ischemia (60minutes), animals were assessed for neurological deficits. Ischemic brain edema was investigated by brain water content detection. Another three groups of animals at the same conditions were studied to evaluate the possible disruption of BBB by Evans blue extravasation technique.

 Results: When sham operated rats had no motor deficit, induction of ischemia in ischemic group, seriously caused impairment of motor functions and neurological deficit score(NDS) of ischemic group was 2.67±0.42. Pretreatment with enalapril (0.03mg/kg) significantly reduced NDS and improved motor dysfunctions (1.5±0.34, P<0.05). Induction of ischemia seriously caused edema formation in right (ischemic) hemisphere of the brain in ischemic group (4.1±0.4 percent). Pretreatment with enalapril (0.03mg/kg) significantly decreased edema compared to ischemic group (1.89±0.23 percent). Extravasation of Evans blue in right side of the brain in ischemic group (12.48±1.94 μg/g) was significantly more than sham group. Pretreatment with enalapril (0.03mg/kg) had protective effects on BBB function and decreased Evans blue extravasation by 44.5 percent (6.92±1.46 μg/g).

 Conclusion: RAS�inhibition by enalapril reduces ischemic brain edema formation by protecting the integrity of BBB and reducing its permeability following focal cerebral ischemia in rat. Pre-ischemic inhibition of RAS activity may reduce ischemic brain injury by ameliorating edema formation.

  Background & Objectives: Hypertension is one of the most important and common health problems in societies. Hypertension is often asymptomatic and can be simply treated. Many of drugs are available for treatment of hypertension i ncluding d iuretics, beta blockers, blockers of calcium channel, angiotensin-converting enzyme inhibitors, angiotensin receptor antagonists, alpha blockers and arterial dilators. This research was performed to evaluate the efficacy of some of these drugs on the hypertension. This may help to choose an appropriate medication for the treatment of stage 2 hypertension.

  Methods: A total of 150 patients with hypertension who were not under antihypertensive treatment and didn’t have contraindications for using hydrochlorothiazide , enalapril and atenolol were randomly allocated into three groups. These groups received atenolol 50 mg daily, hydrochlorothiazide 50 mg daily and enalapril 5 mg twice daily, respectively . After three weeks blood pressure of patients was measured and results were analyzed using SPSS.

  Results: Atenolol reduced systolic blood pressure (26.7±6.7 mm Hg 16.1%), diastolic blood pressure (10.3±1.2 mm Hg 10.4%) and mean arterial blood pressure (16.1±6.4 mm Hg 13.1%). Enalapril reduced systolic blood pressure (30.6±8.8 mm Hg 17.4%), diastolic blood pressure (11.5±4.4 mm Hg 11.4%) and mean arterial blood pressure (17.9±7.0 mm Hg 14.2%). Hydrochlorothiazide reduced systolic blood pressure (25.1±5.8 mm Hg 14.6%), diastolic blood pressure (9.2±2.3 mm Hg 9.3%) and mean arterial blood pressure (14.5±6.4 mm Hg 11.8%).

  Conclusion: Despite recommendations the use of hydrochlorothiazidein the treatment of hypertension, seems lower effect only use of this drug groups in comparison with other groups, and maybe add this category to other drugs and combined treatment is better than monotherapy with these groups .

Background & objectives: Ischemic stroke has complex pathophysiology and its treatment with single neuroprotective drugs has so far failed. Combination therapy could produce amplified protective effects via different mechanisms. We examined the neuroprotective effects of enalapril and/or alpha tocopherol against sensorimotor dysfunctions of ischemic stroke.

Methods: Forty male Sprague-Dawley rats were randomly divided into five groups (n=8): sham, control ischemic, enalapril (0.03 mg/kg), alpha tocopherol (30mg/kg) and enalapril plus alpha tocopherol treated groups. Transient focal cerebral ischemia (90 min) was induced by occlusion of the left middle cerebral artery that followed by 24 h reperfusion periods. Infarct volumes were detected by TTC coloring technique and sensorimotor dysfunctions investigated by rotarod, grip strength and hotplate tests.

Results: Induction of cerebral ischemia in the control group produced severe neurological sensorimotor deficits in conjunction with considerable cerebral infarctions. Compared with the enalapril or alpha tocopherol groups, the combined treatment significantly improved neurological motor and sensory functions (p=0.038 and p=0.034, respectively) and also reduced the infarct volume (p=0.032).

Conclusion: Administration of alpha tocopherol increased protective effects of enalapril. Enalapril combined with alpha tocopherol can produce an augmented protection against ischemic brain injury, and improvement in sensorimotor dysfunctions.