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BACKGROUND: Studies have confirmed that enalapril can alleviate myocardial injury caused by limb ischemia-reperfusion, but the mechanism of its action has not been reported. OBJECTIVE: To investigate the effect mechanism of enalapril reduction of myocardial injury by ischemia-reperfusion in the rat limb. METHODS: Forty-eight healthy adult male Sprague-Dawley rats were randomly divided into control group, model group, enalapril group and inhibitor group. Except for the normal control group, rats were bundled around the ligation of the posterior limbs with a rubber band for 3 hours, followed by 3-hour reperfusion to establish the model of limb ischemia-reperfusion. Intravenous injection of 0.3 mg/kg LY294002 was given in the inhibitor group 30 minutes before reperfusion. Enalapril group and inhibitor group were given intravenous infusion of enalapril 13 μg/kg/h immediately after reperfusion until the end of reperfusion. An equal amount of normal saline solution was given in the other two groups immediately after reperfusion. After 3 hours of reperfusion, the rats were killed and the myocardial tissue was taken. Myocardial histopathological changes, apoptotic index, apoptosis gene expression and cell conduction pathway protein expression were detected. The study was approved by the Laboratory Animal Ethical Committee of Shenyang Medical College in October 2019 with an approval No. (2019)85. RESULTS AND CONCLUSION: Compared with the model group, myocardial histopathological injury was reduced in the enalapril group. Compared with the enalapril group, myocardial histopathological injury was aggravated in the inhibitor group. Compared with the model group, myocardial apoptosis index (AI) was decreased, Bax expression was downregulated, PI3K, p-Akt and Bcl-2 expression was up-regulated in the enalapril group (P < 0.05). Compared with the enalapril group, myocardial apoptosis index was increased, Bax expression was up-regulated, PI3K, p-Akt and Bcl-2 expression was downregulated in the inhibitor group (P < 0.05). The mechanism by which enalapril reduces limb ischemia-reperfusion caused myocardial injury is related to activating PI3K/Akt signaling pathway and inhibiting cell apoptosis in rats. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of enalapril on angiotensin (Ang) Ⅱ and TGF-β/Smads in renal tissue of spontaneously hypertensive rats (SHR). Methods A total of 20 male SHRs were randomly divided into model group and enalapril group. Ten male Wistar Kyoto rats (WKY) were taken as control group. The dosage of enalapril was 1.05 mg/(kg·d), once a day, for 10 weeks. The model group and the control group were given the same amount of normal saline. Blood pressure was monitored every two weeks regularly. After 10 weeks animals were killed and tissue samples were collected. Urease method was used to detect the blood urea nitrogen (BUN) content. Enzyme-linked immunosorbent assay (ELISA) was used to detect the contents of Ang Ⅱ, serum cystatin C (CysC) and urinary microalbumin (mALB). Masson staining was used to observe the renal pathological changes. Real-time PCR was used to detect the relative mRNA expressions of AngⅡ, transforming growth factor β1(TGF-β1), Smad2, Smad3, CollagenⅠ and Collagen Ⅳ. Results Compared with the control group, the systolic and diastolic blood pressures increased significantly in the model group and enalapril group (P＜0.05). There were no significant differences in the systolic and diastolic blood pressures between the model group and enalapril group (P＞0.05). After drug intervention, compared with the model group, the systolic and diastolic blood pressures decreased significantly in enalapril group (P＜0.05). Compared with the control group, the levels of Ang Ⅱ, BUN, CysC and urinary mALB were significantly increased in the model group (P＜0.05). A large number of blue collagen fibers were deposited in renal tissue, and the relative mRNA expressions of Ang Ⅱ, TGF-β1, Smad2, Smad3, Collagen Ⅰ and Collagen Ⅳ were significantly increased (P＜0.05). Compared with the model group, the level of collagen deposition was significantly reduced in renal tissue, and the above indexes in serum and kidney decreased significantly in enalapril group (P＜0.05). Conclusion Enalapril has a stable hypertensive effect on SHR, and it can alleviate renal fibrosis and improve renal injury caused by hypertension by lowering Ang Ⅱ level and inhibiting the expression of TGF-β/Smads signaling pathway. [ABSTRACT FROM AUTHOR]

Objective To compare the effects of enalapril and simvastatin on bone mineral density and bone metabolism in elderly patients with hypertension and osteoporosis. Methods From July 2013 to September 2015, 126 elderly patients with hypertension and osteoporosis were randomly divided into treatment group (n = 63) and control group (n = 63). Patients in the treatment group were treated with enalapril + simvastatin and those in the control group received enalapril only. Serum levels of osteocalcin (OC), type I collagen C-tcrminal peptide (s-CTX), bone-derived alkaline phosphatase (BAP), tartrate - resistant phosphatase - 5b (TRACP - 5b) and bone mineral density (lumbar spine anteroposterior, femoral neck, forearm and greater trochanter) were measured at baseline and 6 months after treatment. Results There were no significant differences between the two groups in bone mineral density and bone metabolic index at baseline (P> 0.05). After treatment, OC. BAP and BiMD of lumbar spine, femoral neck, forearm and greater trochanter significantly increased, and the levels of s-CTX and TRACP-5b significantly decreased (P < 0.05) in both groups. After treatment, OC, BAP, s-CTX, TRACP-5b and BMD of lumbar spine, femoral neck, forearm and greater trochanter of the treatment group were significantly better than those in the control group (P <0. 05). Conclusion Elderly hypertensive patients with osteoporosis received enalapril and simvastatin treatment for 6 months had significantly greater increase in bone mineral density than oral administration of enalapril alone. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To systematically review the clinical safety and efficacy of valsartan and enalapril in treatment of chronic heart failure, so as to provide reference for the clinical drug use. METHODS: Embase, Pubmed, Cochrane library, CBM, CNKI, VIP and Wanfang database were retrieved for RCTs of valsartan and enalapril in patients with chronic heart failure. Meta-analysis was performed by using RevMan 5.3.RESULTS: Totally 14 literatures were involved , including 1665 patients with chronic heart failure. According to Meta-analysis, there were no significant differences between valsartan and enalapril group in changes of the total number of valid cases, left ventricular ejection fraction, left ventricular diastolic internal diameter or volume and left ventricular systolic end-stage or volume(P>0.05). The incidence of adverse drug reactions in valsartan group was significantly lower than that of enalapril group, with statistically significant difference (RR=0.45, 95%CI=0.31-0.66, P<0.01). CONCLUSIONS: Current evidence shows that valsartan and enalapril have the same effect in treatment of chronic heart failure, yet valsartan is better than enalapril in the safety. [ABSTRACT FROM AUTHOR]