Disease relevance of lisinopril

• A case of fulminant hepatitis in a patient taking lisinopril for 5 weeks for arterial hypertension is reported [1].
• CONCLUSIONS: Lisinopril alleviated chronic pancreatitis and fibrosis in male WBN/Kob rats [2].
• Lisinopril and renal failure [3].
• Effect of lisinopril on progression of retinopathy in normotensive people with type 1 diabetes. The EUCLID Study Group. EURODIAB Controlled Trial of Lisinopril in Insulin-Dependent Diabetes Mellitus [4].
• We assessed the effects of lisinopril, an angiotensin-converting enzyme (ACE) inhibitor, on spontaneously occurring chronic pancreatitis [2].

Psychiatry related information on lisinopril

• In the whole study population, high-dose lisinopril led to a trend in risk reduction of all-cause mortality (primary end-point P=0.128) and a significant risk reduction in all-cause mortality plus hospitalization (principal secondary end-point P=0.002) [5].
• ACE inhibition with lisinopril effectively reduced systolic and diastolic pressure in the office (P less than 0.001), at rest (P less than 0.002), during mental stress (P less than 0.003), cold pressor test (P less than 0.003), and reaction time task (P less than 0.05) [6].
• From patients' self-assessments of quality of life, lisinopril was found to be superior to metoprolol in some aspects of emotional, cognitive and social functioning [7].
• The hypotensive effects of three different angiotensin converting enzyme (ACE) inhibitors (captopril, enalapril, and lisinopril) and two angiotensin II (AII) analogues ([Sar1Ile5Ala8]AII and [Sar1Ile5Thr8]AII) were compared in conscious, freely-moving Brattleboro rats after 14 h of water deprivation [8].
• A total of 466 patients with essential hypertension were treated with lisinopril alone (monotherapy group, n = 360) or with a combination of lisinopril with trichlormethiazide (combination therapy group, n = 106) for 1 year [9].

High impact information on lisinopril

• High doses of lisinopril suppressed the overexpression of TGF-beta1 mRNA measured by reverse-transcription polymerase chain reaction (RT-PCR) and decreased the number of alpha-SMA-positive cells (activated pancreatic stellate cells) in the pancreas [2].
• RESULTS: Lisinopril attenuated gross alterations in the pancreas [2].
• Comparison of vasopeptidase inhibitor, omapatrilat, and lisinopril on exercise tolerance and morbidity in patients with heart failure: IMPRESS randomised trial [10].
• Adult Schönlein-Henoch purpura after lisinopril [11].
• It had an alkaline pH optimum and was inhibited by lisinopril, potato carboxypeptidase inhibitor, ethylenediaminetetraacetic acid, 1,10-phenanthroline, and 8-hydroxyquinoline [12].

Chemical compound and disease context of lisinopril

• To evaluate the benefit of angiotensin converting enzyme inhibition in reversing this interstitial and vascular remodeling in the rat with genetic spontaneous hypertension (SHR) and established left ventricular hypertrophy (LVH), we treated 14-week-old male SHR with oral lisinopril (average dose, 15 mg/kg/day) for 12 weeks [13].
• METHODS AND RESULTS: In 206 essential hypertensive subjects with left ventricular hypertrophy (LVH), we measured clinic supine BP, 24-hour ABP, and left ventricular mass index (LVMI, echocardiography) before and after 12 months of treatment with lisinopril (20 mg UID) without or with hydrochlorothiazide (12.5 or 25 mg UID) [14].
• Differences between nisoldipine and lisinopril on glomerular filtration rates and albuminuria in hypertensive IDDM patients with diabetic nephropathy during the first year of treatment [15].
• PATIENTS AND METHODS: Thirty-one hypertensive patients with LV hypertrophy were treated with ACEI (16 with enalapril; 15 with lisinopril) for 1 year [16].
• A randomized, parallel, double-blind study was performed with lisinopril, a long-acting angiotensin-converting enzyme inhibitor, versus captopril, a shorter-acting angiotensin-converting enzyme inhibitor, in the treatment of congestive heart failure [17].

Biological context of lisinopril

• High-dose lisinopril reduced arterial blood pressure and normalized right ventricular and LV weight and resulted in a substantial reduction of 1-year mortality, whereas the low dose did not (1 year mortality: placebo, 56.3%; low dose, 53.3%; high dose, 22.9%, P < .0001 versus low dose and versus placebo) [18].
• Administration of lisinopril attenuated the development of left and right ventricular hypertrophy in this model and was accompanied by an attenuation of the upregulation of the ACE, collagen type I-alpha, and vimentin mRNAs [19].
• In addition, the inhibitory potency of captopril (C), enalaprilat (E), and lisinopril (L) for each domain was assayed by hydrolysis of Hip-His-Leu [20].
• AER at 2 years (adjusted for baseline AER) was 51.3% lower on lisinopril than placebo in the II genotype patients (95% CI, 15.7 to 71.8; P = 0.01), 14.8% in the ID group (-7.8 to 32.7; P = 0.2), and 7.7% in the DD group (-36.6 to 37.6; P = 0.7) [21].
• Pharmacokinetics of lisinopril [22].

Anatomical context of lisinopril

• Thus, in SHR with LVH and adverse structural remodeling of the cardiac interstitium, lisinopril reversed fibrous tissue accumulation and medial thickening of intramyocardial coronary arteries and restored myocardial stiffness and coronary vascular reserve to normal [13].
• Relative to placebo, lisinopril therapy was associated with only minimal, statistically insignificant changes in hemodynamics, a significant increase in myocardial beta-receptor density, no significant (P < .05) changes in cardiac or systemic adrenergic drive, and no detectable change in lymphocyte beta-receptor density [23].
• The effects of endothelium removal and of local incubation with the converting enzyme inhibitor lisinopril (ICI Pharma 209000) on the carotid compliance (CC) were compared with the effects of total abolition of the vascular smooth muscle tone by potassium cyanide [24].
• Angiotensin-converting enzyme was purified from human lung, kidney, testis, blood plasma, and seminal plasma using a facile two-step protocol which included affinity chromatography on Sepharose-bound lisinopril followed by either gel filtration or hydroxylapatite chromatography [25].
• Neutralization of TGFbeta1 by anti-TGFbeta1 or lisinopril resulted in less collagen deposition and less accumulation of myofibroblasts, and levels of active TGFbeta1 and ACE were reduced in thyroids of treated mice compared with those of untreated controls [26].

Associations of lisinopril with other chemical compounds

• Comparative effects of low and high doses of the angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. ATLAS Study Group [27].
• Additional groups of infarcted rats were treated with the ACE inhibitor lisinopril or the AT1 receptor antagonist ZD7155, each separately and in combination with icatibant [28].
• Neither dose affected LV ACE activity and ACE mRNA levels as determined by competitive polymerase chain reaction, whereas LV ANF mRNA levels were significantly reduced by high-dose lisinopril [18].
• The aim of our study was to evaluate whether inhibition of ACE (lisinopril 10-20 mg/day) can reduce the rate of decline in kidney function more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg/day), usually in combination with a diuretic [29].
• ACEH activity is inhibited by EDTA but not by classical ACE inhibitors such as captopril, lisinopril, or enalaprilat [30].
• The authors note that lisinopril contained lipid peroxidation, elevated tissue glutathione levels, and influenced the activity of antioxidant enzymes such as catalase and glutathione peroxidase [31].

Gene context of lisinopril

• Ang II content in pouch tissue was measured by radioimmunoassay following HPLC separation while its capacity to generate Ang II was assessed in tissue bath, with and without exogenous Ang I or lisinopril, an ACE inhibitor [32].
• VEGF levels were not altered by lisinopril treatment [33].
• After long-term treatment with lisinopril, levels of cardiotrophin-1 mRNA were not changed, although it morphologically prevented the development of left ventricular hypertrophy [34].
• Chronic EtOH ingestion also increased the levels of the NADPH oxidase subunit, gp91phox, an effect that was attenuated by lisinopril, but had no effect on lung p22phox or p47phox levels [35].
• The results of this preliminary study suggest that lisinopril affects plasma f-T and SHBG concentrations [36].

Analytical, diagnostic and therapeutic context of lisinopril

• The detergent-solubilized enzyme was purified to apparent electrophoretic homogeneity by affinity chromatography using lisinopril or potato carboxypeptidase inhibitor as an affinity ligand [12].
• Ambulatory blood pressure is superior to clinic blood pressure in predicting treatment-induced regression of left ventricular hypertrophy. SAMPLE Study Group. Study on Ambulatory Monitoring of Blood Pressure and Lisinopril Evaluation [14].
• Lisinopril was added in increasing doses until a maximal dose of 40 mg/d. Titration stopped when target proteinuria (< 1 g/d) was reached or further dose titration was not tolerated because of side effects [37].
• Lisinopril probably undergoes glomerular filtration, tubular secretion, and tubular reabsorption [22].
• CONCLUSIONS: Myocardial perfusion reserve and maximal coronary flow improved in asymptomatic patients with hypertension-induced LVH after long-term treatment with lisinopril but not with losartan [38].

References