Drugs online research references
Can J Cardiol. 1988 Jun-Aug;4(5):237-42.
Correlation of left ventricular hypertrophy and its regression by lisinopril with salt-induced hypertension.
Snedden W, Fernandez PG, Fernandez D, Vasdev S, Rabin EZ.
Division of Clinical Pharmacology, Faculty of Medicine, Memorial University of Newfoundland, St John's.
The interaction of salt with hypertension-induced left ventricular hypertrophy and its reversal by inhibition of angiotensin converting enzyme were studied in salt sensitive and salt resistant Dahl rats. Eight-week-old rats were fed either a low or high salt diet for three weeks. The colonies were then further divided and either treated with lisinopril or given no treatment for 11 weeks. Untreated salt sensitive rats had higher blood pressures than salt resistant animals. Left ventricular weight and wall thickness in both untreated salt sensitive groups was higher than in the resistant groups. Therapy lowered blood pressures in all groups but those of the high salt group remained higher than the low salt group. Reduction of left ventricular weight and wall thickness took place in either strain only when salt intake was low. Right ventricular and atrial weights were largely unaffected either by salt intake or drug therapy. Plasma renin activity increased and aldosterone levels decreased with lisinopril therapy in all groups except the salt sensitive, high salt group where both remained unchanged at low levels. Lisinopril was effective in reducing blood pressure and left ventricular hypertrophy, but both effects were severely impaired by high salt intake. The major determinant of left ventricular hypertrophy appeared to be afterload, as shown by a good correlation between left ventricular mass and systolic blood pressure, but there was some indication of a possible independent hypertrophic action of salt.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2842021&dopt=Abstract
Surgery. 1994 Apr;115(4):495-502.
Both lisinopril and verapamil reduced platelet-derived growth factor-A chain mRNA levels in human saphenous vein endothelial cells stimulated by thrombin.
Yamaguchi M, Gallati H, Baur W, Cruess DF, Sharefkin JB.
Department of Surgery, New England Medical Center Hospitals, Boston, Mass.
BACKGROUND. Both angiotensin-converting enzyme inhibitors and calcium channel blockers decrease postinjury intimal thickening in vivo, but their mechanisms of inhibitory action are unclear. Expression of the gene for platelet-derived growth factor (PDGF), a smooth-muscle mitogen, in endothelial cells (ECs) after vessel injury has been postulated to cause intimal thickening. In this study, we tested whether lisinopril, an angiotensin-converting enzyme inhibitor, or verapamil, a calcium channel blocker, would suppress the PDGF gene expression in stimulated human saphenous vein ECs. METHODS. Drugs were added to replicate EC cultures 30 minutes before adding 10 units/ml alpha-thrombin. Changes in PDGF-A chain mRNA levels were measured by Northern blot analysis or reverse transcription-polymerase chain reaction method. PDGF-AA homodimer in conditioned media was measured by ELISA. RESULTS. Lisinopril attenuated the induction by thrombin of PDGF-A chain mRNA levels significantly in human ECs at doses of 10(-6) mol/L and 10(-5) mol/L (p < 0.05) and appeared to decrease PDGF-AA homodimer released in conditioned medium. Verapamil also reduced thrombin induction of PDGF-A chain mRNA levels significantly at a dose of 10(-5) mol/L (p < 0.05) and appeared to reduce PDGF-AA homodimer secretion. CONCLUSIONS. These data suggest that one means by which lisinopril and verapamil both suppress intimal thickening might be inhibition of PDGF-A chain gene expression in ECs regrowing over vessel injury areas that are sites of thrombin generation.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8165541&dopt=Abstract
Rev Prat. 1990 Oct 11;40(23 Suppl):53-8.
[The value of lysinopril in cardiac insufficiency]
[Article in French]
Lambert M, Luccioni R.
Service de cardiologie, hopital de la Timone, Marseille.
Owing to its original pharmacokinetic profile, lisinopril can be taken once a day, independently of meals, providing a 24-hour inhibition of the angiotensin-converting enzyme. Lisinopril is a potent angiotensin-converting enzyme inhibitor. Administered in doses of 2.5 to 20 mg per day, it improves the functional and haemodynamic state of patients whose congestive heart failure is refractory to the digitalis-diuretic treatment. The drug is well tolerated, and no severe side-effects have been reported. Lisinopril seems to be at least as effective as captopril in congestive heart failure, and it has over the latter the advantage of a once a day dosage therapy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2176346&dopt=Abstract
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