Drugs online research references
Res Commun Mol Pathol Pharmacol. 1997 May;96(2):125-36.
Free radical scavenging properties of alacepril metabolites and lisinopril.
Noda Y, Mori A, Packer L.
Department of Molecular and Cell Biology, University of California, Berkeley 94720-3200, USA.
Alacepril is an inhibitor of the angiotensin converting enzyme (ACE), and is commonly used as an antihypertensive. In this study, the effects of alacepril, its metabolites, desacetylalacepril and captopril, and also lisinopril, which has no sulfhydryl group in the structure, on free radicals were examined in vitro, using an ESR method. Superoxide and hydroxyl radical scavenging activities of alacepril metabolites, desacetylalacepril and captopril, were observed, whereas lisinopril hardly scavenged the superoxide or the hydroxyl radicals. Alacepril and its metabolites did not scavenge nitric oxide, but lisinopril showed slight scavenging activity. These findings suggest that the biological action of alacepril may be partly due to the antioxidant effect of its metabolites, having a sulfhydryl group.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9226747&dopt=Abstract
word match zestril online literature
Fundam Clin Pharmacol. 1997;11(3):221-30.
Response of large and small vessels to alpha and beta adrenoceptor stimulation in heart failure: effect of angiotensin converting enzyme inhibition.
Mulder P, Compagnon P, Devaux B, Richard V, Henry JP, Elfertak L, Wimart MC, Thibout E, Comoy E, Mace B, Thuillez C.
Department of Pharmacology, VACOMED, IFRMP no 23, Rouen University Medical School, France.
The increased sympathetic drive in chronic heart failure (CHF) might provoke vascular adrenoceptor desensitization, which, together with endothelial dysfunction, could contribute to the altered vasomotor tone seen in CHF. We investigated 1) whether CHF alters the responses mediated by alpha and beta adrenoceptors in small and large peripheral arteries, and 2) the effect of angiotensin-converting enzyme (ACE) inhibition. Rats with CHF (coronary artery ligation) were treated with placebo or the ACE inhibitor lisinopril (10 mg/kg/d) starting 7 days after ligation. Responses to phenylephrine (alpha 1 agonist), salbutamol (beta 2 agonist) as well as acetylcholine (endothelium-dependent), were assessed after 3 months in isolated and pressurized segments of the abdominal aorta, the femoral and the mesenteric arteries. In animals with hemodynamic signs of CHF, neither the vasoconstrictor responses to phenylephrine nor the vasodilator response to salbutamol were affected. In contrast, the dilator response to acetylcholine of both small arteries, but not that of the aorta, was impaired. Furthermore, CHF did not modify vessel structure. While lisinopril did not modify the responses to adrenergic agonists, it normalized the response to acetylcholine. Furthermore, ACE inhibition reduced vascular media cross sectional area and collagen density. Thus, the unchanged arterial responsiveness to adrenoceptor agonists does not indicate any vascular adrenoceptor desensitization, while endothelial dependent vasodilation of small arteries is impaired in CHF. ACE inhibition does not modify the response to adrenergic stimuli, prevents endothelial dysfunction and induces both cardiac and vascular remodeling, which probably contribute to the effect ACE inhibitors have on exercise tolerance and survival.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9243253&dopt=Abstract
word match zestril online literature
Can J Physiol Pharmacol. 1997 May;75(5):363-7.
Effects of lisinopril on intercellular resistance of guinea pig ventricular myocytes.
Daleau P, Turgeon J.
Department of Pharmacology, Faculty of Medicine, Laval University, Ste-Foy, QC, Canada.
Previous reports have suggested that angiotensin converting enzyme (ACE) inhibitors are able to modulate intercellular resistance through an ACE-independent action. Therefore, the aim of our study was to determine whether the ACE inhibitor lisinopril would modulate intercellular resistance of guinea pig ventricular myocytes. Junctional resistance was measured using the double patch-clamp technique in eight cell pairs at baseline and during superfusion with 10(-4) M lisinopril. In these cell pairs, mean junctional resistance (+/-SEM) measured at baseline (14.5 +/- 3.8 M omega) was unchanged (15.0 +/- 3.6 M omega; p > 0.05) during lisinopril even after a 25-min exposure to the drug (n = 3). As well, a 20-min exposure to 10(-6) M lisinopril from the intracellular milieu did not modify the junctional resistance. In conclusion, this study demonstrates that modulation of junctional resistance independent of drug-related ACE inhibition is not observed with lisinopril.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9250369&dopt=Abstract
word match zestril online literature
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