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Life Sci. 2000 Aug 11;67(12):1409-21.
Poor regression of myocardial hypertrophy following concomitant chronic alcohol ingestion and angiotensin converting enzyme (ACE) inhibition.

Patel VB, Sandhu G, Dunn MJ, Mantle D, Rodrigues LM, Griffiths JR, Wassif W, Richardson PJ, Preedy VR.

Department of Biochemistry, Wake Forest University School of Medicine, Winston-Salem, NC, USA.

In the following study we examined the combined effect of chronic alcohol administration and anti-hypertensive drug treatment in spontaneously hypertensive rats (SHR). SHR were fed alcohol for six weeks while taking the angiotensin converting enzyme (ACE) inhibitor lisinopril. After six weeks, protein synthesis rates, contractile protein levels and protease activities were examined in control; alcohol; control+lisinopril; alcohol+lisinopril groups. Lisinopril treatment significantly reduced left ventricular mass, protein content and contractile proteins in control rats, but these effects were not as pronounced in alcohol+lisinopril rats. Protein synthesis rates in both mixed and myofibrillar fractions were not significantly different in any of the 4 groups. The enzyme activities of the proteases cathepsin D and dipeptidyl aminopepetidase I increased in control+lisinopril rats, however, this effect was not evident in alcohol+lisinopril rats. Contractile proteins identified by one-dimensional electrophoresis showed that lisinopril treatment reduced all contractile proteins in control rats. However, in alcohol+ lisinopril rats, myosin heavy chain was higher than in control+lisinopril rats. In summary, alcohol ingestion impairs the regression of the hypertrophic myocardium in SHR on ACE-inhibitor treatment, which was reflected by altered protein metabolism. This study suggests that successful anti-hypertensive treatment may not be achieved if alcohol misuse is evident.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10983838&dopt=Abstract

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grape.med.tottori-u.ac.jp

It has been reported that a host develops a marked fever under dehydrated conditions compared with normally hydrated conditions (11). The present study was carried out to investigate whether ANG II is involved in the enhancement seen in dehydrated rats of the fever induced by bacterial endotoxin. The results showed that intravenous injection of bacterial endotoxin produced a fever in dehydrated rats (rats deprived of water for 24 h) that was significantly greater than that seen in normally hydrated rats. In contrast, dehydration had no effect on the fever induced by intravenous interleukin-1beta (IL-1beta). Under dehydrated conditions, the enhanced endotoxin-induced fever was significantly inhibited by the angiotensin-converting enzyme inhibitor lisinopril, but the IL-1beta fever was not. These results suggest that the dehydration-induced enhancement of endotoxin fever is due, at least in part, to the action of ANG II, which elicits an increased production of pyrogenic cytokines such as IL-1.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11004022&dopt=Abstract

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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

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