Drugs online research references
Orv Hetil. 2000 Aug 20;141(34):1867-72.
[Effectiveness of Lisinopril in the treatment of heart failure]
[Article in Hungarian]
Ruszty L, Nagy A, Szonyi T, Valyi P, Poor F, Takacs J, Zalavary I.
I. Belgyogyaszati Osztaly, Jahn Ferenc Del-pesti Korhaz Budapest.
A prospective study was performed in patients (30 M, 16 F, mean age of 56.0 +/- 9.2 [42-73] years) with congestive heart failure to assess the efficacy of lisinopril during a 16 weeks treatment period. Changes in clinical signs, functional capacity, blood pressure, heart rate, echocardiographic parameters, exercise duration, laboratory data and quality of life were measured. After a 2-week run-in period starting daily dose of study drug was 5 mg, and an increase of medication was considered at 4 weeks. At the end of the study mean daily dose of lisinopril was 15.1 +/- 6.2 mg. Improvement of NYHA status by 2 grades was observed in 4 cases (9%), by 1 grade in 24 cases (51%), there was no change in 17 cases (38%), and worsening was observed in 1 case (2%). During the study both systolic (p = 0.001) and diastolic blood pressure (p = 0.0006) decreased significantly, the changes in pulse rate were not significant. Left ventricular end systolic (p = 0.001) and end diastolic (p = 0.003) dimensions decreased, ejection fraction rose by 4.4% (p = 0.0002). One patient was removed from the study because of drug-induced cough. Comparison of all the laboratory data for pre and post-study periods did not reveal any significant difference. Patients treated with lisinopril improved significantly for clinical, haemodynamic, echocardiographic and quality of life parameters, with few adverse experiences, good tolerability and once-daily dose.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11006711&dopt=Abstract
J Cell Physiol. 2000 Nov;185(2):253-9.
Apoptosis of lung epithelial cells in response to TNF-alpha requires angiotensin II generation de novo.
Wang R, Alam G, Zagariya A, Gidea C, Pinillos H, Lalude O, Choudhary G, Oezatalay D, Uhal BD.
The Cardiovascular Institute, Michael Reese Hospital and Medical Center, Chicago, Illinois, USA.
Recent work from this laboratory demonstrated that apoptosis of pulmonary alveolar epithelial cells (AEC) in response to Fas requires angiotensin II (ANGII) generation de novo and binding to its receptor (Wang et al., 1999b, Am J Physiol Lung Cell Mol Physiol 277:L1245-L1250). These findings led us to hypothesize that a similar mechanism might be involved in the induction of AEC apoptosis by TNF-alpha. Apoptosis was detected by assessment of nuclear and chromatin morphology, increased activity of caspase 3, binding of annexin V, and by net cell loss inhibitable by the caspase inhibitor ZVAD-fmk. Purified human TNF-alpha induced dose-dependent apoptosis in primary type II pneumocytes isolated from rats or in the AEC-derived human lung carcinoma cell line A549. Apoptosis in response to TNF-alpha was inhibited in a dose-dependent manner by the nonselective ANGII receptor antagonist saralasin or by the nonthiol ACE inhibitor lisinopril; the inhibition of TNF-induced apoptosis was maximal at 50 microgram/ml saralasin (101% inhibition) and at 0.5 microgram/ml lisinopril (86% inhibition). In both cell culture models, purified TNF-alpha caused a significant increase in the mRNA for angiotensinogen (ANGEN), which was not expressed in unactivated cells. Transfection of primary cultures of rat AEC with antisense oligonucleotides against ANGEN mRNA inhibited the subsequent induction of TNF-stimulated apoptosis by 72% (P < 0.01). Exposure to TNF-alpha increased the concentration of ANGII in the serum-free extracellular medium by fivefold in A549 cell cultures and by 40-fold in primary AEC preparations; further, exposure to TNF-alpha for 40 h caused a net cell loss of 70%, which was completely abrogated by either the caspase inhibitor ZVAD-fmk, lisinopril, or saralasin. Apoptosis in response to TNF-alpha was also completely inhibited by neutralizing antibodies specific for ANGII (P < 0.01), but isotype-matched nonimmune immunoglobulins had no significant effect. These data indicate that the induction of AEC apoptosis by TNF-alpha requires a functional renin/angiotensin system (RAS) in the target cell. They also suggest that therapeutic control of AEC apoptosis in response to TNF-alpha is feasible through pharmacologic manipulation of the local RAS. Copyright 2000 Wiley-Liss, Inc.
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med.kitasato-u.ac.jp
We have previously reported that the renal kallikrein-kinin system suppressed the development of deoxycorticosterone acetate (DOCA)-salt hypertension. Kinins were degraded in the kidney mainly by carboxypeptidase Y (CPY)-like kininase. Blockade of renal kinin degradation may reduce hypertension in the developmental stage. We constructed an antisense oligonucleotide against rat CPY homologue (5'-CAT-CTC-TGC-TTC-CTT-GTG-TC-3', AS) and its randomized control oligonucleotide (5'-TCC-TTC-CTG-CTT-GAG-TTC-CT-3', RC), and prepared an HVJ-liposome complex that prolongs and increases the effectiveness of the antisense oligonucleotide. Antisense oligonucleotide was transfected (25 nmole rat(-1), in terms of nucleotide) into the kidney from the renal artery. Blood pressure was measured through a catheter inserted into the abdominal aorta. Mean blood pressure (MBP) in DOCA-salt treated (for 2 weeks) Sprague Dawley strain rats was 130+/-3 mmHg (n=11), and was reduced significantly (P<0.05) more by AS transfection (122+/-4 mmHg, n=6) than by RC treatment (137+/-6 mmHg, n=5) 4 days after the transfection. This reduction in MBP was accompanied by increased urinary sodium excretion (AS, 8.4+/-1.5 mmole day(-1); RC, 4.6+/-0.5 mmole day(-1), P<0.05) and a reduction in urinary CPY-like kininase activity. Ebelactone B (5 mg kg(-1), twice a day, p.o.), an inhibitor for urinary CPY-like kininase, also reduced MBP and induced natriuresis to the same degree as AS. Lisinopril, an inhibitor for angiotensin converting enzyme (ACE) failed to reduce the elevated MBP. These results suggest that CPY-like kininase may have more contribution than ACE to degrade kinin in the kidney, and that knockdown of CPY-like kininase in the kidney may partly prevent rat DOCA-salt hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11030733&dopt=Abstract
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