Drugs online research references
Clin Exp Pharmacol Physiol. 1989 May;16(5):417-24.
Atrial natriuretic peptide levels in congestive heart failure in man before and during converting enzyme inhibition.
Crozier IG, Nicholls MG, Ikram H, Espiner EA, Yandle TG.
Department of Cardiology, Princess Margaret Hospital, Christchurch, New Zealand.
1. To determine the response of plasma atrial natriuretic peptide (ANP) to treatment with an angiotensin converting enzyme (ACE) inhibitor in heart failure, seven patients (NYHA Functional Class III-IV) were studied before and after the addition of ramipril to maintenance digoxin and diuretic treatment. 2. Baseline arterial ANP levels were raised, but fell during ramipril treatment in parallel with changes in both haemodynamic recordings (arterial pressure, pulmonary artery diastolic pressure, and right atrial pressure) and hormone levels (angiotensin II and aldosterone). 3. Coronary sinus ANP, measured in three patients, was greater than concomitant arterial levels, and the coronary sinus ANP secretion rate was calculated to be between 15 and 119 pmol/min. 4. These results demonstrate that improvement in haemodynamic function during ACE inhibitor treatment is associated with a decline in elevated ANP levels, and support the concept that atrial stretch or pressure regulates the secretion of atrial peptides in man.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2527656&dopt=Abstract
J Mol Cell Cardiol. 1996 Mar;28(3):643-54.
Nitric oxide mitigates leukocyte adhesion and vascular leak after myocardial ischemia.
Kupatt C, Zahler S, Seligmann C, Massoudy P, Becker BF, Gerlach E.
Department of Physiology, University of Munich, Germany.
Tissue edema is a facet of ischemia/reperfusion injury in many organs, polymorphonuclear leukocytes (PMN) presumably playing a contributory role. We studied the intracoronary adhesion of PMN and its effect on vascular permeability during reperfusion in isolated guinea-pig hearts. After a global ischemia of 15 min duration. PMN (10(7)) were infused into the coronary system during the first minute of reperfusion. PMN adhesion was measured as difference of applied PMN and those recovered in the effluent perfusate. Coronary permeability was assessed by measuring the rate of transudate formation (TF) on the epicardial surface, before as well as 5, 15 and 30 min after ischemia. Experiments were also performed in the presence of the NO-synthase inhibitor nitro-L-arginine (10 microM) and the ACE-inhibitor ramiprilat (2 microM), the latter known to enhance endogenous nitric oxide formation. Furthermore, the radical scavenger uric acid (0.5 mM) was applied either before and during ischemia or starting after PMN application. Ischemia/reperfusion increased coronary PMN adherence from 23 +/- 1% (basal) to 33 +/- 2%. Whereas ischemia alone did not influence TF (about 100 microliters/min during reperfusion), postischemic PMN infusion led to progressive TF. With nitro-L-arginine, PMN adhesion rose to 45 +/- 3%; TF increased to 212 +/- 30 microliters/min. In contrast, ramiprilat caused post-ischemic adhesion and TF to decline to basal values. In the presence of uric acid (UA) PMN adhesion declined to 26 +/- 2%, however, the subsequent increase in TF after withdrawal of UA was not markedly attenuated. On the other hand, infusion of UA after application of PMN caused a significant decrease of TF. The extracellular antioxidants SOD/catalase were without effect. As shown using luminol enhanced chemiluminescence. No was able to scavenge oxygen free radicals released by activated PMN. These findings indicate that enhanced PMN adhesion in reperfusion leads to an increase in coronary permeability. Scavenging of oxygen free radicals with NO or UA appears to mitigate both, postischemic PMN adhesion and PMN-induced vascular injury, even after adhesion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9011647&dopt=Abstract
Eur J Pharmacol. 1989 Jul 18;166(2):157-64.
Ramiprilat attenuates the local release of noradrenaline in the ischemic myocardium.
Carlsson L, Abrahamsson T.
Department of Pharmacology, University of Goteborg, Sweden.
The effects of the converting enzyme inhibitors ramiprilat and enalaprilat on ischemia-induced release of noradrenaline (NA) were examined in the isolated perfused rat heart, submitted to 30 min of total flow restriction followed by 5 min of reperfusion. Ramiprilat (2.6 nM-2.6 microM) caused a concentration-dependent decrease in the efflux of NA at reperfusion. The maximal effect (about 70% reduction) was observed at a concentration of 26 nM. In contrast, enalaprilat (10 nM-10 microM) caused no reduction in NA efflux until at a high concentration (10 microM, NA efflux reduced by about 20%). Moreover, the prodrugs ramipril and enalapril (added to the perfusion medium) were without any significant effects on ischemia-induced NA release. Both the angiotensin II receptor antagonist saralasin (0.1 microM) and bradykinin (0.1 and 1 nM) caused marked reductions in ischemic NA efflux. However, when indomethacin (10 microM) was added to the perfusion medium, the effects of bradykinin (1 nM) and ramiprilat (26 nM) on NA efflux were abolished. Likewise, in the presence of angiotensin II (0.1 microM) the effect of ramiprilat was no longer evident. The magnitude of cellular injury, expressed as efflux of creatine kinase during reperfusion, was reduced by bradykinin (0.1 and 1 nM) and by ramiprilat (by about 55% at 2.6 microM). It is concluded that ramiprilat, at therapeutically relevant concentrations, attenuates the ischemia-induced mobilization of NA via a reduction in local angiotensin II production and/or bradykinin degradation. The lack of effect of enalaprilat in this model may reflect differences between converting enzyme inhibitors regarding tissue accumulation or the potency of local enzyme inhibition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2792189&dopt=Abstract
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