Drugs online research references
Arzneimittelforschung. 1988 Apr;38(4):531-6.
Antihypertensive and angiotensin converting enzyme inhibitory activities of a novel dihydrobenzofuran analogue.
Hamilton TC, Howlett DR, Longman SD, Markwell RE, Norton J, Summers DR, Wilson C.
Beecham Pharmaceuticals Research Division, Harlow, Essex, UK.
1. The biochemical and pharmacological profiles of the novel, orally active angiotensin converting enzyme (ACE) inhibitor, N-[N-[[4-(2, 3-dihydro-2-benzofuranyl)-1-(ethoxycarbonyl)]butyl]-(s)-alanyl]- (s)-proline (BRL 36378), have been compared with those of enalapril and captopril. 2. In the conscious sodium deficient spontaneously hypertensive rat, BRL 36378 and enalapril (0.3-10 mg/kg orally) produced comparable falls in blood pressure; at 3 mg/kg orally, captopril was less active than BRL 36378 and enalapril. 3. In the anaesthetised spontaneously hypertensive rat, enalapril was slightly more potent than BRL 36378 as an inhibitor of angiotensin I (AI) pressor responses whilst BRL 36378 was about twice as potent as captopril in this test (i.v. route used). BRL 36378 and enalapril were equipotent as potentiators of bradykinin depressor responses. 4. In the anaesthetised Wistar rat, the maximum inhibition of AI pressor responses by 0.1 microgram/kg i.v. BRL 36378 and captopril was achieved sooner than after the same dose of enalapril. The inhibitory effect of captopril subsided completely by 40-50 min but the maximum effects of BRL 36378 and enalapril persisted for at least 60 min. 5. In the conscious renal hypertensive cat, captopril was slightly more potent than BRL 36378 or enalapril as a blood pressure lowering agent, over 1-10 mg/kg orally. BRL 36378 was more potent than enalapril as an inhibitor of AI induced pressor responses in this model. Captopril possessed similar inhibitory activity to BRL 36378 although minor differences in time course were apparent.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2840917&dopt=Abstract
Eur Heart J. 1989 Nov;10 Suppl F:97-100.
Coronary vasodilation induced by intracoronary enalaprilat: an argument for the role of a local renin-angiotensin system in patients with dilated cardiomyopathy.
Foult JM, Tavolaro O, Antony I, Nitenberg A.
Chu Xavier Bichat, Paris, France.
Although indicated by several experimental studies, the presence of a renin-angiotensin system has not been demonstrated in the human heart. The influence of a local renin-angiotensin system on the coronary vessels may be difficult to establish after oral or intravenous administration of an angiotensin converting-enzyme inhibitor, since coronary blood flow depends greatly on the loading conditions of the left ventricle. To avoid such a situation, our study consisted in a direct bilateral intracoronary infusion of enalaprilat in patients with dilated cardiomyopathy and normal coronary arteries (mean ejection fraction = 32 +/- 11%, n = 12). This intracoronary infusion (0.05 mg min-1, 1 ml min-1 in each coronary artery) resulted in no significant change of the systemic resistances (20.6 +/- 5.6 to 22.0 +/- 5.1 mmHg l-1 min), rate-pressure product (10,974 +/- 2630 to 10,214 +/- 2486) or myocardial oxygen consumption (21.08 +/- 6.37 to 22.10 +/- 6.42 ml min-1). Despite these steady haemodynamic conditions, intracoronary enalaprilat provoked a significant elevation of coronary sinus blood flow (181 +/- 73 to 214 +/- 79 ml min-1, P less than 0.001) with a reduction of coronary resistance (0.51 +/- 0.17 to 0.41 +/- 0.15 mmHg ml-1 min, P less than 0.001), and no significant alteration in plasma renin activity or plasma aldosterone. The results of this intracoronary infusion of enalaprilat demonstrate that this angiotensin converting-enzyme inhibitor has significant coronary vasodilator properties, which can be evidenced without stimulating the peripheral renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2559850&dopt=Abstract
Nephron. 1996;73(4):664-9.
Sex chromosomes do not influence renal injury in borderline hypertensive rats.
Van Liew JB, Feld LG.
Department of Medicine, State University of New York at Buffalo, School of Medicine and Biomedical Schiences, N.Y., USA.
The present study was undertaken to investigate whether the development of proteinuria in the borderline hypertensive rat (BHR) is influenced by the Y chromosome and to determine if the onset of proteinuria in the BHR is delayed when blood pressure is lowered with enalapril, an angiotensin I converting enzyme inhibitor. Male F1, rats were the first-generation offspring of the mating of spontaneously hypertensive (SHR) females and Wistar-Kyoto (WKY) males and the mating of SHR males and WKY females. At 20 weeks of age, enalapril (125 mg/l) was added to the drinking water. Untreated BHR and enalapril-treated BHR (BHRE) were followed to 90-100 weeks of age. Urine was collected every 10-20 weeks for determination of protein, albumin, and nitric oxide (NO2/NO3) metabolite excretion. Indirect blood pressure in BHR from both crosses was approximately 175 mm Hg from 20 to 90-100 weeks of age. Enalapril lowered blood pressure by about 30 mm Hg, but was ineffective in reducing urinary protein or albumin excretion rates at any age. Urinary excretion of nitric oxide metabolites was similar in all groups at all time periods. There were significant differences in the percent of glomerulosclerosis between the two matings. Based on these results, renal injury in the BHR is not associated with the Y chromosome and can be dissociated from hypertension. Further studies using congenic and transgenic technology will be necessary to identify functions of genes and associations with hypertension in order to understand the kidney disease in this model of hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8856266&dopt=Abstract
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