Benazepril Group Research Articles

RETRACTED ARTICLE: Comparison of cardioprotective effects using salvianolic acid B and benazepril for the treatment of chronic myocardial infarction in rats

The aim of this study was to compare the cardioprotective effects of salvianolic acid B (Sal B) and the angiotension-converting enzyme inhibitor, benazepril, in rats with chronic myocardial infarction (MI) that resulted from a coronary artery ligation for 4 weeks. The rats were divided into four groups: those undergoing a sham operation; a MI group; a MI+SalB group (100 mg/kg by a gavage, once a day for 4 weeks); a MI+benazepril group (10 mg/kg by a gavage, once a day for 4 weeks). The following parameters were measured: echocardiographic, hemodynamic and hemorheological changes, angiogenesis, infarct size and cardiac remodeling and the messenger ribonucleic acid (mRNA) of vascular endothelium growth factor (VEGF). Rats treated with SalB or benazepril manifested the following: (1) marked improvements in echocardiographic, hemodynamic and hemorheological parameters; (2) significant reduction of infarct size; (3) significantly attenuated heart, kidney and lung hypertrophies, left ventricular (LV) dilatation and fibrosis. The unique effects of SalB were angiogenesis and augmented VEGF expression in the border and remote noninfarcted left ventricular area. These results suggest that both SalB and benazepril exerted beneficial cardioprotective effects in our experimental system, but that the modality of Sal B was different from that of benazepril. The additional beneficial effects of Sal B relative to benazpril, augmenting VEGF expression and promoting angiogenesis, may result in improved myocardial microcirculation.

Transforming growth factor- 1 is associated with kidney damage in patients with essential hypertension: renoprotective effect of ACE inhibitor and/or angiotensin II receptor blocker

Evidence suggests that transforming growth factor-beta1 (TGF-beta(1)) is associated with target organ damage in hypertension. This study aimed to investigate the relationship between TGF-beta(1) levels and kidney damage and renoprotective effects of angiotensin-converting enzyme inhibitor and/or angiotensin II type 1 receptor blocker in patients with essential hypertension (EH). A total of 156 patients with EH were enrolled and grouped according to albumin-to-creatinine ratio (ACR). Of these, 90 patients with EH underwent a 12-week antihypertensive trial with administration of benazepril, valsartan or both. Serum TGF-beta(1), plasma angiotensin (Ang) II and urinary albumin were quantified by immunoassays. Serum TGF-beta1, plasma Ang II and ACR were highly elevated in patients with EH (P < 0.01). There was a positive correlation between serum TGF-beta1 levels and ACR (r = 0.53, P < 0.01). Significant decreases in TGF beta1 and ACR were obtained in all groups at the end of 12-week antihypertensive therapy compared to the baseline values, with the combined group to a greater extent (P < 0.01). Plasma Ang II levels were significantly decreased in the benazepril group but increased in the valsartan group (P < 0.05) while no significant change was observed in the combined group. TGF-beta(1) is highly elevated and strongly associated with urinary albumin excretion in patients with EH. Treatment with benazepril or valsartan attenuates serum TGF-beta(1) levels and microalbuminuria with the combined therapy receiving the greater effect. TGF-beta(1) could be a potential surrogate marker in monitoring the development and progression of kidney damage in EH.

Concerns about "Comparative adverse cardiac effects of pimobendan and benazepril monotherapy in dogs with mild degenerative mitral valve disease: a prospective, controlled, blinded and randomized study".

Concerns about "Comparative adverse cardiac effects of pimobendan and benazepril monotherapy in dogs with mild degenerative mitral valve disease: a prospective, controlled, blinded and randomized study".

Comparative Adverse Cardiac Effects of Pimobendan and Benazepril Monotherapy in Dogs with Mild Degenerative Mitral Valve Disease: A Prospective, Controlled, Blinded, and Randomized Study

Background: Pimobendan (PIMO) is an inodilator that may have some beneficial effects in canine degenerative mitral valve disease (MVD). However, little information is available about its cardiac effects in dogs without systolic myocardial dysfunction. Hypothesis: Compared to benazepril (BNZ), an angiotensin‐converting enzyme inhibitor, PIMO may worsen valve regurgitation in early canine MVD. Animals: Twelve Beagles with asymptomatic MVD were randomized into 2 groups (n = 6) receiving BNZ or PIMO at dosages of 0.25 mg/kg PO q24h and q12h respectively, for 512 days. Methods: The study followed a blinded, randomized, prospective, and parallel group design. After day 512, the dogs were necropsied, and cardiac histopathology was performed in a blinded manner. Results: A significant treatment effect was observed as soon as day 15 with increased systolic function in the PIMO group by comparison to baseline value as assessed by fractional shortening (P &lt; .0001) and tissue Doppler variables (P= .001). Concurrently, the maximum area and peak velocity of the regurgitant jet signal increased (P &lt; .001), whereas these variables remained stable in the BNZ group. Histologic grades of mitral valve lesions were more severe in the PIMO group than in the BNZ group. Moreover, acute focal hemorrhages, endothelial papillary hyperplasia, and infiltration of chordae tendinae with glycosaminoglycans were observed in the mitral valves of dogs from the PIMO group but not in those of the BNZ group. Conclusions and Clinical Importance: PIMO has adverse cardiac functional and morphologic effects in dogs with asymptomatic MVD. Additional investigation in dogs with symptomatic MVD is now warranted.

Clinical evaluation of imidapril in congestive heart failure in dogs: results of the EFFIC study

The clinical efficacy and safety of imidapril were evaluated in dogs that presented with mild to severe congestive heart failure (New York Heart Association stage II to IV) by comparing the success rate of imidapril with a positive control by a non-inferiority approach. This good, clinical practice compliant, multicentre study (EFFIC study) enrolled 142 client-owned dogs and was conducted in 20 locations in France, Belgium and Germany. Dogs of various breed, age and weight were included in the study. These dogs were randomised into two groups that were treated for 84 days with either the test product, imidapril, or the positive control, benazepril, and followed up in parallel over this period. Both treatments were administered at a dose of 0.25 mg/kg once a day with the possibility of doubling this dose to 0.5 mg/kg if considered necessary from a clinical point of view. In addition, concomitant treatment was given to dogs presenting with pulmonary oedema and/or ascites, supraventricular tachyarrhythmia and/or dilated cardiomyopathy. The evolution of the New York Heart Association stage and the "functional signs" score were evaluated as primary efficacy criteria. The success rate in the imidapril group was 66 compared with 68 per cent in the benazepril group. Regarding safety, 35 dogs in each group experienced at least one adverse event. Nine dogs in each group experienced at least one serious adverse event. The difference between these results was not statistically significant. Imidapril is as efficacious and safe as the reference product, benazepril.

Comparative Adverse Cardiac Effects of Pimobendan and Benazepril Monotherapy in Dogs with Mild Degenerative Mitral Valve Disease: A Prospective, Controlled, Blinded, and Randomized Study

Pimobendan (PIMO) is an inodilator that may have some beneficial effects in canine degenerative mitral valve disease (MVD). However, little information is available about its cardiac effects in dogs without systolic myocardial dysfunction. Compared to benazepril (BNZ), an angiotensin-converting enzyme inhibitor, PIMO may worsen valve regurgitation in early canine MVD. Twelve Beagles with asymptomatic MVD were randomized into 2 groups (n = 6) receiving BNZ or PIMO at dosages of 0.25 mg/kg PO q24h and q12h respectively, for 512 days. The study followed a blinded, randomized, prospective, and parallel group design. After day 512, the dogs were necropsied, and cardiac histopathology was performed in a blinded manner. A significant treatment effect was observed as soon as day 15 with increased systolic function in the PIMO group by comparison to baseline value as assessed by fractional shortening (P < .0001) and tissue Doppler variables (P = .001). Concurrently, the maximum area and peak velocity of the regurgitant jet signal increased (P < .001), whereas these variables remained stable in the BNZ group. Histologic grades of mitral valve lesions were more severe in the PIMO group than in the BNZ group. Moreover, acute focal hemorrhages, endothelial papillary hyperplasia, and infiltration of chordae tendinae with glycosaminoglycans were observed in the mitral valves of dogs from the PIMO group but not in those of the BNZ group. PIMO has adverse cardiac functional and morphologic effects in dogs with asymptomatic MVD. Additional investigation in dogs with symptomatic MVD is now warranted.

Benazepril vs enalapril treatment of mild to moderate essential hypertension of old patients in district

目的 比较贝那普利与依那普利治疗老年轻、中度高血压的疗效和安全性.方法将116例社区老年轻、中度高血压病患者随机、单盲分为两组,其中贝那普利组58例,依那普利组58例,治疗8周,并从两组随机抽20例于治疗前及治疗8周末行24 h动态血压检测.结果治疗8周后,两组药物均能有效的降低血压,有效率贝那普利组为94.82%,依那普利组为84.48%,组间比较差异无显著意义(P＞0.05).贝那普利组的谷/峰值收缩压为60.5%,舒张压为57.7%;依那普利组分别为55.2%和52.9%.不良反应发生率贝那普利组为10.34%,依那普利组为18.79%,差异有显著意义(P＜0.05).结论贝那普利更适合社区老年轻、中度高血压病的治疗。

Amlodipine/benazepril combination therapy for hypertensive patients nonresponsive to benazepril monotherapy

Background Most patients with hypertension require two or more antihypertensive medications to achieve blood pressure (BP) goals. This double-blind study compared the efficacy and safety of high-dose combinations of amlodipine besylate (5 mg and 10 mg) and benazepril hydrochloride (40 mg) to benazepril hydrochloride (40 mg) alone in hypertensive patients not adequately controlled with benazepril hydrochloride (40 mg) monotherapy. Methods After a 2-week washout period and a 4-week lead-in period with benazepril 40 mg daily, patients with a mean sitting diastolic BP ≥95 mm Hg (i.e., nonresponders to benazepril 40 mg) were randomly assigned to active treatment with either a combination of amlodipine 5 mg and benazepril 40 mg for 4 weeks followed by a forced titration to amlodipine 10 mg and benazepril 40 mg for an additional 4 weeks, or to benazepril 40 mg alone for 8 weeks. Results The mean reduction in sitting BP from baseline (on benazepril) to endpoint (after 8 weeks of treatment) was 17/14 mm Hg with amlodipine/benazepril and 5/7 mm Hg with benazepril ( P < .0001). The percentage of patients who met the diastolic BP response criteria (<90 mm Hg at endpoint or ≥10 mm Hg decrease from baseline) was 80% in the amlodipine/benazepril group and 45% in the benazepril group ( P < .0001). The incidence of adverse events was infrequent and comparable for both treatment groups. Conclusion High-dose amlodipine/benazepril combination therapy (5 mg/40 mg and 10 mg/40 mg) is an effective, safe, and well-tolerated treatment option for hypertensive patients who do not respond adequately to benazepril alone.

Effect of benazepril amlodipine combination on left ventricular hypertrophy in hypertensive type 2 diabetic patients

P-138 Key Words: Diabetes, Amlodipine, Amlodipine Benazepril Combination

Effect of different angiotensin converting enzyme inhibitors on coronary collateral circulation

To observe the effects of different angiotensin converting enzyme inhibitors (ACEI) on coronary collateral circulation. Twenty-four healthy dogs underwent measurement of distolic aortic pressure (DAP) and ligation of the left anterior descending coronary artery. The distolic coronary pressure (DCP) and retrograde blood flow (Qret) were measured. Five days after the operation the dogs were randomly divided into three groups of 8 dogs: benazepril group (benazepril 10 mg qd); captopril group (captopril 12.5 mg bid) and control group (starch tablet was given). Thirty days after the operation a reflux catheter was inserted to measure the DCP and Qret again. Then the dogs were killed and their hearts were taken out to examine the pathologic changes. The angiotensin converting enzyme (ACE) activity levels in plasma and myocardium were examined by FAPGG spectrophotometry. (1) In the captopril group the plasma ACE activity was (24.1 +/- 0.6) U/L 10 days after medication, and 24.3 +/- 0.6 U/L twenty-five days after medication, both significantly lower than that before medication [(57.6 +/- 0.8) U/L, both P < 0.01]; in benazepril group the plasma ACE activity was (24.4 +/- 0.4) U/L ten days after medication, and (24.0 +/- 0.5) U/L 25 days after medication, both significantly lower than that before medication [(59.5 +/- 1.3) U/L, both P < 0.01]. The plasma ACE activity levels of captopril and benazepril groups, especially of the benazepril group, after medication were significantly lower than that of the control group. The tissue ACE activity levels of the captopril and benazepril groups were lower than that of the control group. (2) The values of DCP in the control and captopril group were higher after medication than before medication. A tendency of decrease of DCP was shown in the benazepril group, however, without statistical significance. (3) In the control group Qcol was (2.01 +/- 0.31) ml/min 25 days after medication, significantly than that before medication [(0.91 +/- 0.15) ml/min], the corresponding values in captopril group were (2.24 +/- 0.46) ml/min and (0.88 +/- 0.13) ml/min respectively in the captopril group and (3.18 +/- 0.27) ml/min and (0.89 +/- 0.11) ml/min respectively in the benazepril group with the value 25 days after in the benazepril group being the highest. (4) 30 days after operation collateral circulation was established in the ischemic myocardium in all 3 groups. The microvessel density in the ischemic zone of myocardium was higher than that in the nonischemic zone in all 3 groups. The microvessel density in the ischemic zone of myocardium was greater in the benazepril group than in the captopril and control groups. There was no difference in microvessel density between the captopril group and control group. Benazepril increases the microvessel density and collateral flow, promotes the creation of collateral circulation in ischemic area, but captopril has not such effects.

Randomized prospective study of effects of benazepril in renal transplantation: an analysis of safety and efficacy

Background. Prolonging the survival of transplanted kidneys is one of major tasks of modern nephrology. Angiotensin-converting enzyme inhibitors (ACEIs) compose a class of antihypertensive agents that has established efficacy in the treatment of hypertension and in slowing the progression of diabetic nephropathy and chronic glomerulonephritis. ACEIs are not widely accepted as a standard medication in the treatment of hypertension in renal transplant recipients because of the potential risk for decreased renal blood flow and glomerular filtration rate associated with a single kidney and concomitant cyclosporin use. Methods. We undertook a prospective randomized study of ACEI (benazepril) treatment in 76 posttransplant patients to determine the safety, efficacy, and side-effect profile of benazepril. Forty-one patients were assigned to the benazepril group and 35 patients were assigned to the control group. Results. The mean arterial blood pressure at a 12-month follow-up was lower than that at the time of initiation of benazepril or control therapy, with a decrease from 101 ± 10 mmHg to 94 ± 7 mmHg (P < 0.05) in the benazepril group and from 102 ± 12 mmHg to 94 ± 10 mmHg in the control group after 12 months of treatment. The serum creatinine concentrations did not change throughout the follow-up period. Conclusions. Benazepril was demonstrated to be an effective antihypertensive without any unfavorable effects on graft function. A significant antiproteinuric effect of benazepril was observed in patients with overt proteinuria. Further follow-up of this patient population will contribute to the establishment of the long-term renoprotective effect of benazepril in renal allograft recipients.

Relationship of collagen content, intimal thickening and angiotensin II level of iliac arteries after balloon injury in rabbits

OBJECTIVE: To investigate the relationship of collagen content intimal thickening and angiotensin II level of iliac arteries after balloon injury in rabbits. METHODS Fifty male New Zealand white rabbits were randomly devided into 6 groups: losartan groups, benazapril groups and control groups for 4 weeks or 8 weeks. Every rabbit underwent endothelial debridement of the right iliac artery. lorsartan (15 mg/kg/d) and benazapril (5 mg/kg/d) were orally administrated respectively in losartan groups and benazepril groups from 5 days before until 4 weeks or 8 weeks after balloon injury. RESULTS: Collagen content and intimal area of rabbit iliac arteries were increased after balloon injury. After intervention for 4 weeks with losartan and benazapril, collagen content was decreased in losartan and benazapril groups than in control group 23.58+/-6.16 % and 22.67+/-10.20 % compared with 35.20+/-7.25 % respectively, P<0.05. After intervention for 8 weeks, collagen content was significantly decreased (20.69+/-11.16)% and 25.41+/-11.00 % compared with 42.69+/-13.99 % respectively, P<0.05; Intimal area and intimal to medial area ratio were also decreased in losartan and benazapril groups than in control group; Lumen area was increased in losartan and benazapril groups than in control group(0.79+/-0.25)mm2 and (0.76+/-0.28)mm2 compared with (0.62+/-0.27)mm2 P<0.05; Tissue angiotensin II level was increased in losartan group (516.31+/-70.79)pg/mg.pro compared with (410.72+/-100.11)pg/mg.pro, P<0.05, and decreased in benazapril group than in control group (340.62+/-67.69)pg/mg.pro compared with (410.72+/-100.11)pg/mg.pro, P<0.05. There were close correlation between tissue angiotensin II level and intimal area, or between tissue angiotensin II level and intimal to medial area ratio, or and collagen content in benazapril group, respectively, P<0.05. Conclusion (1) Collagen protein is a dynamic participant in vascular injury. (2) Tissue renin angiotensin system may play an important role in collagen accumulation, intimal thickening and vascular injury after angioplasty. (3) Losartan and benazapril reduce vascular collagen content and inhibit intimal thickening after balloon injury.

The effects of antihypertensive agents on the survival rate of polycystic kidney disease in Han:SPRD rats.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary renal disorder in humans. Hypertension is one of the major complications, and its control might affect the renal survival and disease mortality. Suitable antihypertensive agents have been discussed based on clinical and animal studies, but no definitive conclusion has been reached. Generally, therefore, all antihypertensives are indiscriminately treated as if providing the same level of blood pressure control. In this study, the blood pressure control of two antihypertensives was investigated using a rat model of ADPKD in humans. Twenty-four male Hannover-Sprague Dawley (Han:SPRD) rats were divided into three groups: a group receiving amlodipine (6 mg/day), a group receiving benazepril (6 mg/day) and an untreated control group. Blood pressure, body weight, and urinary protein excretion were regularly measured up to week 52. Amlodipine and benazepril significantly decreased blood pressure and urinary protein excretion to the same degree. Moreover, a remarkably prolonged survival rate was observed in both groups (at week 52, the survival rate was 25% in controls, 50% in the amlodipine group, and 50% in the benazepril group). Examination at autopsy revealed that enlarged cysts were prevalent in the renal tissue of both experimental all three groups, suggesting that the cystic disease had reached the end-stage in all the animals. In conclusion, both amlodipine and benazepril significantly improved blood pressure control, urinary protein excretion, and survival rate, possibly due to their enhancement of renal survival.

Pilot study to evaluate a water displacement technique to compare effects of diuretics and ACE inhibitors to alleviate lower extremity edema due to dihydropyridine calcium antagonists

Combination therapy is required in many patients to achieve goal blood pressure (BP). Calcium antagonists are highly effective antihypertensive drugs in a broad range of demographic groups. Yet, higher doses are associated with an increased frequency of lower extremity edema. The purpose of our open label, single-center clinical trial was to evaluate the use of concomitant pharmacologic therapies to attenuate the lower extremity edema associated with dihydropyridine calcium antagonists therapy using a water displacement technique. Forty-seven patients received 5 mg/day of oral amlodipine for a period of 6 weeks after a 4-week wash-out off of all antihypertensive medications to establish baseline BP. They were then randomized to receive either an additional 5 mg of amlodipine, 25 mg of hydrochlorothiazide (HCTZ), or 20 mg of benazepril for an additional 6 weeks. Blood pressure determinations and water displacement measurements were obtained at the end of the 4-week placebo wash-out period, after 6 weeks of 5 mg/day of oral amlodipine therapy, and after an additional 6 weeks of 5 mg of amlodipine and randomized drug therapy. Adjusted BP reductions (based on pretreatment BP) were −6.8/−3.8 mm Hg for the 10-mg amlodipine group, −9.9/−8.2 mm Hg for the amlodipine (5 mg)/HCTZ (25 mg) group, and −26.2/−16.4 mm Hg for the amlodipine (5 mg)/benazepril (20 mg) group ( P < .0167, group 3 v group 1 diastolic BP, which was statistically significant by the improved Bonferroni method). Seventeen of the 47 patients developed at least a 10% increase in lower extremity edema water displacement in response to 5 mg/day of oral amlodipine therapy (36.2%). Adding 5 mg of amlodipine to a baseline of 5 mg of amlodipine resulted in no net change in lower extremity edema (+58.0 mL, +0.6% change, n = 5). Adding 25 mg of HCTZ reduced lower extremity edema by a mean of 136.3 mL (−11.1% change, n = 4). Benazepril reduced water displacement by 204.4 mL (−14.3% change, n = 8). Our pilot study indicates that adding an angiotensin converting enzyme inhibitor to a dihydropyridine calcium channel blocker is the most effective way to not only reduce systolic and diastolic BP but also attenuate lower extremity edema. Due to the inherent daily variability of lower extremity edema, power calculations indicate many patients ( n = 702, 356 in each group) would be needed to compare the antiedema efficacy of the angiotensin converting enzyme inhibitor and the thiazide diuretic.

Effects of benazepril alone and in combination with hydrochlorothiazide in comparison with felodipine extended release in elderly patients with mild-to-moderate essential hypertension

The aim of this study was to assess the efficacy and tolerability of two antihypertensive regimens—one using benazepril, eventually combined with hydrochlorothiazide in nonresponders, and the other using titration of felodipine extended release (ER)—in elderly patients with hypertension. After a 2-week washout period, 236 patients (127 men and 109 women aged 65 to 80 years) with mild-to-moderate essential hypertension (systolic blood pressure [SBP] ⩾160 mm Hg and diastolic blood pressure [DBP] ⩾95 mm Hg), were given benazepril 10 mg once daily (n = 118) or felodipine ER 5 mg once daily (n = 118) for 4 weeks, according to a multicenter, randomized, double-masked design. At the end of this treatment period, patients responding to treatment were kept at the same dose of their respective randomized drug for an additional 8 weeks. The nonresponders were given the fixed combination benazepril 10 mg plus hydrochlorothiazide 12.5 mg or felodipine ER 10 mg. Patients were examined at the end of the washout period and every 4 weeks thereafter. At each visit, sitting SBP and DBP were measured with a mercury sphygmomanometer and heart rate by radial pulse palpation. Adverse events were recorded. Both benazepril and felodipine ER were similarly effective in reducing SBP and DBP. No significant differences between the two treatment groups were observed in the mean decreases in blood pressure or in the number of percentage of patients with successful responses to treatment. Both treatments were well tolerated; the incidence of drug-related side effects, however, was slightly but significantly higher in the felodipine ER-treated group than in the benazepril group (14.4% vs 8.5%). In conclusion, benazepril 10 mg given as monotherapy, or as a fixed combination with hydrochlorothiazide in nonresponders, and felodipine ER 5 mg, titrated to 10 mg in nonresponders, were both effective and well tolerated in elderly patients with hypertension.

Treatment of patients with essential hypertension: amlodipine 5 mg/benazepril 20 mg compared with amlodipine 5 mg, benazepril 20 mg, and placebo

This multicenter, double-masked, randomized, parallel-group study compared the efficacy, tolerability, and safety of amlodipine 5 mg/benazepril 20 mg, amlodipine 5 mg, benazepril 20 mg, and placebo in patients with essential hypertension. After a placebo run-in period, 308 patients (all white) were randomized to treatment groups and took medication once daily for 8 week. Blood pressure was measured after 4 and 8 weeks of treatment in the 23- to 26-hour period after dosing. Patients wore a noninvasive blood pressure monitor for 24 hours before randomization and before the final visit. Investigators recorded adverse experiences at randomization and at study weeks 4 and 8, and obtained specimens for laboratory testing at randomization and at study week 8. Three hundred seven patients were evaluated for efficacy, and 308 for tolerability and safety. At end point (the last postrandomization measurement for each patient), the reduction in mean sitting diastolic blood pressure with the amlodipine 5 mg/benazepril 20 mg treatment was statistically significantly greater than with any comparative therapy. The results of 24-hour monitoring showed that the amlodipine/benazepril treatment, unlike monotherapy, maintained the hourly mean diastolic blood pressure at ≤90 mm Hg. A responder rate of 87.0% was observed with amlodipine 5 mg/benazepril 20 mg versus 67.5%, 53.3%, and 15.8% with amlodipine, benazepril, and placebo, respectively. This difference between the amlodipine/benazepril treatment group and each comparative single-agent treatment group was statistically significant. Drug-related adverse events occurred in 15.6% of patients in the amlodipine/benazepril group and in 24.7%, 6.5%, and 11.7% of patients in the amlodipine, benazepril, and placebo groups, respectively. Edema occurred less often in the amlodipine/benazepril group than in the amlodipine group. Overall, once daily therapy with amlodipine 5 mg/benazepril 20 mg provided an antihypertensive effect that was statistically and clinically superior to amlodipine 5 mg alone, benazepril 20 mg alone, and placebo, was well tolerated, and was associated with less edema than the amlodipine treatment.

Safety profile of benazepril in essential hypertension

Data from clinical trials with benazepril suggest that the safety profile of benazepril is similar to that of other angiotensin-converting enzyme (ACE) inhibitors. Treatment-related side effects occurred in 20% of benazepril-treated patients and in 18% of patients receiving placebo. The most commonly reported side effects with benazepril were headache, dizziness, and fatigue. The incidence of side effects was not affected by the degree of hypertension, age, gender, race, dosage, or the degree of renal impairment. Side effects believed to be related to the pharmacologic action of ACE inhibitors as a class include symptomatic hypotension, which occurred at a relatively low rate with benazepril, and hyperkalemia and elevation of serum creatinine, which occurred to the same extent with benazepril as has been noted with other ACE inhibitors. The mechanism of cough as an ACE inhibitor side effect is unknown; the incidence was similar to that with other ACE inhibitors. Rash and taste disturbance have occurred rarely with benazepril. The incidence of neutropenia and of proteinuria was the same in both the benazepril and placebo groups. Renal failure in hypertensive patients treated with benazepril has not been reported. Overall, benazepril is generally well tolerated by hypertensive patients. The incidence of most side effects is comparable to that with other ACE inhibitors and placebo.