benazepril and Hypertrophy--Left-Ventricular

An altered ambulatory blood pressure (BP) and heart rate (HR) profile is related to chronic kidney disease (CKD) and cardiorenal syndrome. In this study, we examined the effects of aliskiren, when added to angiotensin II type 1 receptor blockers, on ambulatory BP and cardiorenal function in CKD. Thirty-six hypertensive CKD patients were randomly assigned to the aliskiren add-on group (n = 18) or the benazepril add-on group (n = 18). Ambulatory BP and cardiorenal function parameters were measured at baseline and 24 weeks after treatment. Compared with the benazepril group, nighttime systolic BP variability in the aliskiren group was lower after treatment. Albuminuria was decreased in the aliskiren group, but not in the benazepril group. In addition, left ventricular mass index (LVMI) was significantly lower in the aliskiren group than in the benazepril group after treatment. In the aliskiren group, multivariate linear regression analysis showed an association between changes in albuminuria and changes in nighttime systolic BP. Furthermore, there were associations between changes in LVMI and changes in daytime HR variability, as well as between changes in LVMI and changes in plasma aldosterone concentration. These results suggest that aliskiren add-on therapy may be beneficial for suppression of renal deterioration and pathological cardiac remodeling through an improvement that is effected in ambulatory BP and HR profiles.

Topics: Aged; Albuminuria; Amides; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Benzazepines; Blood Pressure; Cardio-Renal Syndrome; Female; Fumarates; Heart Function Tests; Heart Rate; Humans; Hypertrophy, Left Ventricular; Kidney Function Tests; Male; Oxidative Stress; Renal Insufficiency, Chronic

Left ventricular hypertrophy, a major cardiovascular risk factor for morbidity and mortality, is commonly caused by arterial hypertension. The renin-angiotensin-aldosterone system may contribute to the pathogenesis of left ventricular hypertrophy. The Assessment of Lotrel in Left Ventricular Hypertrophy and Hypertension Study compared a single-pill combination of amlodipine/benazepril at doses 5.0/20.0 mg, 5.0/40.0 mg, and 10.0/40.0 mg with hydrochlorothiazide/benazepril at doses 12.5/20.0 mg, 12.5/40.0 mg, and 25.0/40.0 mg on the reduction of left ventricular mass index measured by cardiac MRI in stage 2 hypertensive patients over 52 weeks of treatment in a randomized clinical trial. A total of 125 male and female patients, > or =55 years of age, with echocardiographic left ventricular hypertrophy and high-risk hypertension defined as blood pressure > or =160/100 mm Hg or current antihypertensive treatment were enrolled. After 52 weeks of treatment, left ventricular mass index was significantly reduced from baseline with amlodipine/benazepril (mean: 10.16 g/m(2)) or hydrochlorothiazide/benazepril (mean: 6.74 g/m(2); both P<0.0001), with a mean difference between treatment groups of 3.36 g/m(2) (P=0.16). No significant treatment differences were observed in subgroups defined by age, male gender, race, diabetes status, or dose level. However, in female patients, left ventricular mass index reduction was greater with amlodipine/benazepril (P=0.02). Both treatments were well tolerated.

Topics: Aged; Amlodipine; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Calcium Channel Blockers; Diuretics; Dose-Response Relationship, Drug; Double-Blind Method; Drug Combinations; Female; Heart Ventricles; Humans; Hydrochlorothiazide; Hypertension; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging; Male; Middle Aged; Risk Factors; Sex Characteristics; Treatment Outcome

Angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs) increase arterial compliance and decrease left ventricular mass in hypertensive patients. This study examined whether combined therapy has greater arterial and cardiac effects than doubled doses of the individual drugs.. This prospective, randomized, open-label study enrolled 106 patients aged >/=18 years with mild-to-moderate hypertension. Patients were randomized to 5 mg of amlodipine or 20 mg of benazepril for 2 weeks; then, depending on randomization assignment, they were force-titrated to 10 mg of amlodipine or 40 mg of benazepril monotherapy, or to combination amlodipine (5 mg) and benazepril (20 mg) treatment for 22 weeks. Arterial distensibility was assessed using the DynaPulse ambulatory system, and left ventricular mass was assessed by echocardiography.. Combination therapy (0.71% +/- 0.51% mL/mm Hg) increased arterial distensibility more than amlodipine (0.28% +/- 0.69% mL/mm Hg; P =.008) or benazepril (0.39% +/- 0.62% mL/mm Hg; P =.03) monotherapies. Left ventricular mass decreased more with combination treatment (65 +/- 56 g) than with amlodipine (28 +/- 4 g; P <.02); the difference from benazepril (42 +/- 50 g) was not significant.. Combined ACE inhibitor and CCB treatment was more efficacious than high doses of the individual agents in increasing arterial compliance and reducing left ventricular mass. These findings indicate that appropriately selected combinations of antihypertensive drugs might have enhanced cardioprotective effects.

Topics: Adult; Amlodipine; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Calcium Channel Blockers; Drug Therapy, Combination; Female; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Male; Middle Aged; Prospective Studies; Treatment Outcome; Vascular Capacitance; Vascular Resistance

The coexistence of hypertension increases cardiovascular risks and the rate of deterioration of renal function for diabetic patients. For patients with left ventricular hypertrophy (LVH), the use of an angiotensin converting enzyme (ACE) inhibitor is known to be effective and well tolerated and to be protective against chronic renal insufficiency (CRI). However, serious adverse reactions to ACE inhibitors, such as the rapid deterioration of renal function, have been reported, making physicians hesitant to use these agents. To resolve this dilemma, we compared changes in renal function and left ventricular function and the safety and effectiveness of benazepril, an ACE inhibitor, in patients with diabetic nephropathy, with or without LVH. The age, sex, duration of diabetes, levels of blood pressure and blood glucose and rates of creatinine clearance (CrCl) were compared between 36 diabetic patients with LVH and 36 matched diabetic patients without LVH. The rates of CrCl in all patients were between 14 and 35 ml/min, and all patients received an ACE inhibitor before enrollment. The group comprised 43 men and 29 women, with a mean age of 56 +/- 4 years. These patients were divided into three groups, each of which was subdivided into a group with and a group without LVH. Group I (without LVH) or I-L (with LVH) received a half dose of benazepril (2.5 mg daily), Group II (without LVH) or II-L (with LVH) received a normal daily dose of 5 mg benazepril, and Group III (without LVH) or III-L (with LVH) discontinued the administration of the ACE inhibitor. The follow-up period was 1 year and, during the study, blood pressure was maintained at less than 140/90 mmHg. If the blood pressure control was not satisfactory, benidipine, a calcium antagonist, and/or furosemide, a loop diuretic, and/or guanabenz, a central acting antihypertensive agent, were administered. In the diabetic patients with LVH, the administration of a normal dose of benazepril inhibited the decline of renal function and cardiac function (CrCl: 24.2 +/- 1.5 to 22.0 +/- 2.5 ml/min; EF (ejection fraction): 56 +/- 3 to 54 +/- 6%) compared to the other two groups. In patients without LVH, a half dose of benazepril preserved renal function (23.4 +/- 2.6 to 22.0 +/- 3.1 ml/min; EF: 54 +/- 3 to 56 +/- 3%). Discontinuation of the administration of ACE inhibitor led to the further progression of renal dysfunction and decreases in EF in patients with or without LVH. Our results provide some indications for th

Topics: Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Blood Pressure; Circadian Rhythm; Creatine; Diabetic Angiopathies; Diabetic Nephropathies; Dose-Response Relationship, Drug; Echocardiography; Female; Hemoglobins; Humans; Hypertrophy, Left Ventricular; Male; Potassium; Proteinuria

The aim of this study was to compare the effects of an angiotensin-converting enzyme (ACE) inhibitor and alphabeta blocker in combination with a calcium antagonist on the progression of renal function and left ventricular hypertrophy (LVH) in patients with chronic renal insufficiency and hypertension. The 65 subjects in this study were recruited from a cohort of 316 patients. The main criteria for inclusion were echocardiographic diagnosis of LVH (posterior wall thickness >12 mm) and serum creatinine of more than 1.5 mg/dl. Antihypertensive treatments were switched to the combination of amlodipine at a dose of 5 mg and benazepril at a dose of 2.5 mg daily or the combination of amlodipine at a dose of 5 mg and arotinolol at a dose of 20 mg daily at random irrespective of whether or not patients had been previously treated. The follow-up period was 2 years. Systolic and diastolic blood pressure were significantly reduced from 150/90 +/- 15/11 mmHg to 130/75 +/- 11/9 mmHg (ACE) and the levels of serum creatinine were increased significantly from 1.8 +/- 0.3 to 2.0 +/- 0.4 mg/dl (ACE). In the alphabeta-blocker group, these two values were similar and no significant changes were found. PWT was decreased from 14.2 +/- 0.6 to 12.9 +/- 0.3 cm in alphabeta blocker but was not significantly decreased in the ACE inhibitor group. In conclusion, combination therapy with a calcium antagonist and abeta blocker might be effective treatment for hypertensive patients with chronic renal insufficiency and left ventricular hypertrophy.

Topics: Adrenergic alpha-Antagonists; Adrenergic beta-Antagonists; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Blood Pressure; Cohort Studies; Creatinine; Drug Therapy, Combination; Echocardiography; Female; Follow-Up Studies; Humans; Hypertension, Renal; Hypertrophy, Left Ventricular; Kidney Failure, Chronic; Male; Middle Aged; Pilot Projects; Propanolamines; Proteinuria

To assess the comparative effects of benazepril and nitrendipine monotherapies on left ventricular mass index (LVMI) in hypertensive patients with echocardiographically determined left ventricular hypertrophy, patients with diastolic blood pressure (BP) > or = 100 mm Hg were randomized to benazepril, 10 mg, or nitrendipine, 20 mg, both given once or twice daily. After 4 weeks, only the responders (diastolic BP <90 mm Hg) entered a 5-month maintenance period. At baseline, and after 3 and 6 months, LVMI was blindly estimated by means of magnetic resonance imaging (MRI) and, for comparison, by means of echocardiography. Of the 50 randomized patients, three were excluded from the study as nonresponders after 4 weeks; moreover, two patients taking benazepril and one taking nitrendipine discontinued the treatment after 2 months for adverse effects. Both monotherapies reduced systolic and diastolic BP to a similar extent. After 3 months, MRI-estimated LVMI decreased by 21.5 g/m2 in the benazepril and 8.8 g/m2 in the nitrendipine group, with an adjusted mean difference between the two groups of 11.1 g/m2 (95% CI, 7.3-14.8 g/m2; p = 0.0001). After 6 months, it decreased by 23.6 g/m2 and 10.0 g/m2, respectively, with an adjusted mean difference of 11.3 g/m2 (95% CI, 7.5-15.5; p = 0.0001) in favor of benazepril. In conclusion, despite a similar antihypertensive effect, benazepril led to a greater reduction in MRI-measured LVMI than did nitrendipine (-16.2% vs. -7.2%) in hypertensive patients with left ventricular hypertrophy.

Topics: Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Blood Pressure; Calcium Channel Blockers; Echocardiography; Female; Heart Rate; Humans; Hypertension; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging; Male; Middle Aged; Nitrendipine; Prospective Studies; Ventricular Function, Left

To investigate the effects of different drugs on systolic blood pressure (SBP) and left ventricular hypertrophy (LVH) in spontaneously hypertensive rats under cold stress.. A total of 40 male spontaneously hypertensive rats aged 10 weeks (160~200 g) were given adaptive feeding for 7 days at a temperature of 20±1°C and then randomly divided into control group, cold stress group, metoprolol group, amlodipine group, and benazepril group, with 8 rats in each group. SBP, body weight, and heart rate were measured once a week. After the rats were sacrificed by exsanguination, left ventricular weight (LVW) was measured, and left ventricular weight index (LVWI; mg/g) was calculated. Radioimmunoassay was used to measure the concentrations of endothelin-1 (ET-1) and angiotensin-II (Ang-II) in plasma and myocardium, and the chemical method was used to measure the concentrations of nitric oxide (NO) in plasma and myocardium. RT-PCR was used to measure the mRNA expression of endothelin-A receptor.. Compared with the cold stress group, all medication groups showed significant reductions in SBP since week 5 (P<0.05). The cold stress group showed a significant increase in LVWI compared with the control group (3.38±0.27 mg/g vs 2.89±0.19 mg/g, P<0.05). The amlodipine group showed a significant reduction in LVWI compared with the cold stress group (2.98±0.28 mg/g vs 3.38±0.27 mg/g, P<0.05). The cold stress group showed a significant reduction in plasma NO concentration compared with the control group (104.9±19.5 μmol/L vs 129.3±17.8 μmol/L, P<0.05) ; compared with the cold stress group, all the medication groups showed significant increases in blood NO concentration (P<0.05). The cold stress group showed a significant increase in myocardial ET-1 concentration compared with the control group (6.3±1.5 pg/100 mg vs 4.5±1.9 pg/100 mg, P<0.05) ; compared with the cold stress group, the amlodipine group showed a significant reduction in myocardial ET-1 concentration (4.4±1.0 pg/100 mg vs 6.3±1.5 pg/100 mg, P<0.05). The cold stress group had significantly higher mRNA expression of endothelin-A receptor than the control group (0.86±0.23 vs 0.45±0.16, P<0.01) ; compared with the cold stress group, the amlodipine group showed a significant reduction in the mRNA expression of endothelin-A receptor (0.41±0.14 vs 0.86±0.23, P<0.01).. Amlodipine can reduce the increase in SBP and inhibit LVH in spontaneously hypertensive rats under cold stress.

Topics: Angiotensin II; Animals; Benzazepines; Blood Pressure; Cold Temperature; Endothelin-1; Hypertension; Hypertrophy, Left Ventricular; Male; Myocardium; Rats; Rats, Inbred SHR; Stress, Physiological

Benazepril, an angiotensin-converting enzyme (ACE) inhibitor, has been used to treat hypertension, congestive heart failure, and chronic renal failure. However, its biological activity and mechanism of action in inflammation are not fully identified. The present study was designed to determine the in vivo anti-inflammatory effects of benazepril on LV hypertrophy in rats.. LV hypertrophy was produced in rats by abdominal aortic coarctation. They were then divided into the following groups: sham operation; LV hypertrophy; LV hypertrophy+benazepril (1mg/kg in a gavage, once a day for 4 weeks). Both morphological assays (hemodynamic and hemorheological measurement; LV hypertrophy assessment), and molecular assays (protein levels of Collagen type I/III, TNF-α and VCAM-1; TGF-β gene expression; NF-κB or Smad activation; intracellular ROS production) were performed.. The following effects were observed in rats treated with benazepril: (1) marked improvements in hemodynamic and hemorheological parameters; (2) significant reductions in LV hypertrophy, dilatation and fibrosis; (3) significantly attenuated protein levels of Collagen type I/III, TGF-β, TNF-α and VCAM-1, NF-κB or Smad activation, as well as intracellular ROS production.. These results suggest that the anti-inflammatory properties of benazepril may be ascribed to their down-regulation of both NF-κB and TGF-β signaling pathways by acting on the intracellular ROS production in rats with LV hypertrophy, thus supporting the use of benazepril as an anti-inflammatory agent.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Anti-Inflammatory Agents; Aorta; Aortic Coarctation; Benzazepines; Blood Pressure; Collagen Type I; Collagen Type III; Enzyme Activation; Hemodynamics; Hypertension; Hypertrophy, Left Ventricular; Inflammation; Male; NF-kappa B; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Signal Transduction; Smad Proteins; Transforming Growth Factor beta; Vascular Cell Adhesion Molecule-1

To investigate the association between insertion/deletion (I/D) polymorphism of the angiotensin converting enzyme (ACE) gene and the A/B polymorphism of the chymase (CMA) gene with regression of left ventricular hypertrophy (LVH) in patients with essential hypertension and left ventricular hypertrophy. The study subjects had been participants in along-term trial of therapy with an ACE inhibitor.. Follow-up data of 157 patients with essential hypertension and left ventricular hypertrophy were collected. DNA fragments of ACE gene and CMA gene were amplified by PCR and analysed by RFLP. LVDd, IVST and LVPWT were measured by Ultrasonic Cardiogram (UCG).. (1) When long-term treatment with Benazepril was carried out, the blood pressure was markedly decreased and the heart rate was maintained steadily. (2) Regression of left ventricular hypertrophy was improved. (3) The magnitudes of regression of LVM and LVMI during therapy were greater in the DD group than in the II and ID group. No significant differences of other indices were found in the different genotype groups of ACE. (4) No significant differences of all indices were found in the different genotype groups of CMA. (5) No interaction appeared between the genotypes of the ACE and the genotypes of the CMA.. Hypertensive patients with DD genotype were more likely to have regression of left ventricular hypertrophy when treated with ACE inhibitors than patients with other ACE genotypes. No evidence was found to support an association between CMA genotype and regression of LVH in those patients.

Topics: Adult; Angiotensin-Converting Enzyme Inhibitors; Benzazepines; Chymases; Female; Follow-Up Studies; Genotype; Humans; Hypertension; Hypertrophy, Left Ventricular; Male; Peptidyl-Dipeptidase A; Polymerase Chain Reaction; Polymorphism, Genetic; Polymorphism, Restriction Fragment Length; Serine Endopeptidases

Although recent clinical studies have indicated that angiotensin II receptor blocker is as effective in treating heart failure as an angiotensin-converting enzyme inhibitor, it is unknown whether their effects are different. Dahl salt-sensitive rats were treated with an angiotensin-converting enzyme inhibitor benazepril, and an angiotensin II receptor blocker candesartan from 11 weeks old. We examined cardiac geometry and function by echocardiography, and histology and gene expression by high-density oligonucleotide arrays using Affymetrix U34 (Affymetrix, Santa Clara, CA, U.S.A.). Dahl salt-sensitive rats fed a high salt diet showed a marked increase in blood pressure and developed concentric hypertrophy at 11 weeks, followed by left ventricle dilation and congestive heart failure by 20 weeks after birth. Although both medications had only a mild antihypertensive effect, they strongly suppressed the development of cardiac hypertrophy, fibrosis and heart failure to the same extent. Gene expression pattern examined by Affymetrix GeneChip (Affymetrix) is quite different between the two drug groups, indicating that angiotensin II receptor blocker and angiotensin-converting enzyme inhibitor prevent heart failure by different mechanisms.

Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Benzazepines; Benzimidazoles; Biphenyl Compounds; Disease Models, Animal; Echocardiography; Fibrosis; Gene Expression; Gene Expression Profiling; Heart Failure; Hypertension; Hypertrophy, Left Ventricular; Infusions, Parenteral; Male; Oligonucleotide Array Sequence Analysis; Organ Size; Rats; Rats, Inbred Dahl; Receptors, Angiotensin; Sodium Chloride, Dietary; Subcutaneous Tissue; Tetrazoles; Time Factors; Ventricular Function, Left

To evaluate the antihypertensive efficacy of angiotensin converting enzyme inhibitor (ACEI) benazepril in combination with AT1 receptor antagonist valsartan and their effect on left ventricular hypertrophy, renin angiotensin aldosterone system (RAAS) and endoxin in spontaneously hypertensive rat (SHR).. WKY control group (n = 6) and other 4 groups consisted of 24 SHR (14-week-old, male, n = 6): SHR control group, benazepril group, valsartan group, and combination drug therapy group. Systolic blood pressure (SBP) of SHR was measured at the beginning and at the end of 2, 4, 6, and 8 wk of drug intervention. Morphometric determination, renin activities, angiotensin II (Ang II), endoxin, and ATPase activity analysis were performed at the end of 8 week of drug intervention.. SBP, ratio of left ventricular mass (LVM), body weight (BW) (LVM/BW), and transverse diameter of myocardial cell (TDM) of SHR were remarkably decreased after drug intervention, and this decrease was most remarkable in the combination drug therapy group. Renin activities of plasma and myocardium were remarkably increased in drug intervention groups. The levels of Ang II in plasma and myocardium were remarkably increased in valsartan group, decreased in benazepril group and combination drug therapy group. Na(+)-K(+)-ATPase activities in myocardium were remarkably increased and the level of endoxin in myocardium were remarkably decreased as SBP decreased after drug intervention.. Both benazepril and valsartan can decrease SBP of SHR, and cause regression of ventricular hypertrophy. The efficacy of combination drug therapy group is most remarkable among all groups and avoids the side effects of induction of high Ang II levels in plasma and myocardium caused by long-term use of valsartan alone.

Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Benzazepines; Blood Pressure; Drug Therapy, Combination; Hypertension; Hypertrophy, Left Ventricular; Male; Random Allocation; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Tetrazoles; Valine; Valsartan

To assess the effects of benazepril (ACE inhibitor) on arterial blood pressure (ABP) and left ventricular mass index (LVMI).. Nineteen patients (7 men, 12 women) with mean age 38.2 +/- 10.2 years, with mild to moderate hypertension were evaluated. Besides raised blood pressure, the necessary inclusion criterion was the presence of left ventricular hypertrophy detected by echocardiogram. After a wash-out period, all patients were given placebo followed by the active drug benazepril at a dose of 10 mg once a day. For those patients who did not achieve a satisfactory control of the blood pressure (BP) 25 mg of chlorthalidone was added. All patients underwent 180 days of benazepril treatment.. The ABP was gradually controlled as follow: at seated position the systolic BP changed from 156.05 +/- 5.07 mmHg to 129 +/- 3.74 mmHg (p < 0.001) and the diastolic BP from 99.74 +/- 1.59 mmHg to 81.8 +/- 2.27 mmHg (p < 0.001). At orthostatic position the systolic BP changed from 156.9 +/- 5.35 mmHg to 124.28 +/- 5.33 mmHg (p < 0.001) and the diastolic BP from 101.7 +/- 1.34 to 81.36 +/- 2.81 (p < 0.001). The heart rate did not change significantly during the study. The LVMI decreased significantly from 182.4 +/- 9.2g/m2 to 122.6 +/- 4.2g/m2 (p < 0.001).. Our data revealed that 100% of the patients achieved satisfactory degrees of LVMI regression and in 34% there was a normalization of it.

Topics: Administration, Oral; Antihypertensive Agents; Benzazepines; Blood Pressure; Female; Humans; Hypertension; Hypertrophy, Left Ventricular; Male

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Antihypertensive Agents; Benzazepines; Celiprolol; Collagen; Hypertension; Hypertrophy, Left Ventricular; Male; Proteins; Rats; Rats, Inbred SHR; Rats, Inbred WKY; RNA; Verapamil

This study was undertaken to determine the biochemical and left ventricular functional changes associated with reversal of left ventricular hypertrophy (LVH) in spontaneously hypertensive rats (SHR).. Male SHR and normotensive Wistar-Kyoto (WKY) rats, aged 19 weeks, were treated for 3 weeks with vehicle, amlodipine (10 mg/kg), benazepril (10 mg/kg) or the combination of both agents (4 mg/kg amlodipine and 4 mg/kg benazepril). Left ventricular function was assessed while blood was infused rapidly, at pharmacologically reduced and pretreatment mean arterial pressure (MAP).. All treatments reduced MAP and left ventricular mass significantly in SHR. Myocardial protein, RNA and myocardial collagen content were reduced proportionately in all treatment groups in SHR, but not in WKY rats. DNA remained unchanged in all groups. Increased right ventricular mass was produced by amlodipine in both SHR and WKY rats (SHR +11.3%; WKY +9.8%), but this was prevented by cotreatment with benazepril. Right ventricular protein and collagen increased significantly with amlodipine in SHR but not WKY rats, and there were no changes in right ventricular RNA and DNA contents in either strain. Amlodipine improved, benazepril impaired and the combination of both agents maintained left ventricular pumping ability when pressure was increased abruptly to pretreatment levels in WKY rats. In contrast, when afterload was increased abruptly in SHR to pretreatment levels, neither amlodipine nor benazepril affected pumping ability, although it was enhanced by the combination.. These data demonstrate that amlodipine, benazepril and their combination reduced left ventricular mass in SHR. This reversal of LVH was associated with proportional reductions in mycotic protein, RNA and collagen, but not DNA. Therefore, it seems unlikely that LVH reversal with these agents was associated with increased fibrous tissue or impaired left ventricular performance. Finally, addition of the angiotensin converting enzyme inhibitor prevents the increase in right ventricular mass produced by the calcium antagonist.

Topics: Amlodipine; Animals; Benzazepines; Collagen; Drug Combinations; Hemodynamics; Hypertension; Hypertrophy, Left Ventricular; Male; Myocardium; Nucleic Acids; Proteins; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Ventricular Function, Left