Drugs online research references
Biol Neonate. 1992;61(2):124-30.
Placental alterations, intrauterine growth retardation and teratogenicity associated with enalapril use in pregnant rats.
Valdes G, Marinovic D, Falcon C, Chuaqui R, Duarte I.
Department of Nephrourology, School of Medicine, Catholic University, Santiago, Chile.
Enalapril (15 mg/kg/day p.o.) was given to 11 pregnant rats from day 1 to 9 (E1-9) and to 11 rats from day 10 to 20 (E10-20) of pregnancy; 12 rats were the control group. Fifteen animals were sacrificed on day 20 of pregnancy and 19 were allowed to progress into partum. Placentas were smaller in E10-20 rats (-15%, p less than 0.05) and had a simple hypocellular cordonal structure; in E1-9 animals the predominant pattern was a combination of complex and simple structure. At day 20 the fetuses in the treated groups were smaller than the controls (-5% in E1-9 and -16% in E10-20, p less than 0.05); differences disappeared on the 13th day postpartum. Two fetuses from treated mothers presented incomplete skull ossification. We believe this report adds arguments to preclude converting enzyme inhibitors in pregnancy.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1567931&dopt=Abstract
Jpn J Pharmacol. 1994 Oct;66(2):231-40.
Histopathological investigation on salt-loaded stroke-prone spontaneously hypertensive rats, whose biochemical parameters of renal dysfunction were ameliorated by administration of imidapril.
Fujiwara T, Yuasa H, Ogiku N, Kawai Y.
Safety Research Laboratory, Tanabe Seiyaku Co., Ltd., Osaka, Japan.
Our previous studies showed that imidapril prevented the occurrence of cerebral stroke and ameliorated biochemical parameter changes of renal dysfunction at a dose that did not inhibit the progression of hypertension in salt-loaded stroke-prone spontaneously hypertensive rats (SHRSP). To confirm these findings, a histopathological investigation was conducted on the kidney of salt-loaded (from 11 to 16 weeks of age) SHRSP, which was the subject of the preceding study. Their brains and hearts were also examined. Histopathologically, renal lesions such as fibrinoid necrosis and proliferative arteritis of small calibration arteries, necrotizing glomerulitis and tubular degeneration, and cerebral hemorrhage and slight cardial hypertrophy were observed in salt-loaded control SHRSP. The occurrence of these lesions were prevented in a dose-dependent manner by the administration of imidapril (1 and 2 mg/kg/day). Especially, the preventive effects on the renal lesions were apparently noted. Enalapril also prevented these renal lesions, but its preventive effects were weaker than those of imidapril at the same dose (2 mg/kg/day). It became evident from the results of the present and previous studies that imidapril reduced renal biochemical and histopathological injuries.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7869607&dopt=Abstract
Am J Physiol. 1996 Jun;270(6 Pt 2):H1985-92.
Bradykinin pathway is involved in acute hemodynamic effects of enalaprilat in dogs with heart failure.
Barbe F, Su JB, Guyene TT, Crozatier B, Menard J, Hittinger L.
Institut National de la sante et de la Recherche Medicale, Faculte de Medecine, Creteil, France.
To determine the role of the renin-angiotensin system and the bradykinin pathway in the mechanism of action of angiotensin-converting enzyme inhibitors in heart failure, the acute effects of enalaprilat (1 mg/kg) were compared with those of a renin inhibitor (ciprokiren, 1 mg/kg i.v.) in 10 chronically instrumented conscious dogs with heart failure induced by right ventricular pacing (3 wk, 240 beats/min). The effects of enalaprilat and ciprokiren on bradykinin infusion (3, 10, and 30 micrograms/min) and the effects of enalaprilat in the presence of the bradykinin B2 receptor antagonist Hoe-140 (10 micrograms/kg i.v.) were also examined. Both inhibitors significantly decreased mean aortic pressure and increased cardiac output. However, enalaprilat induced significantly greater hemodynamic effects than ciprokiren (mean aortic pressure, -13 +/- 3 vs. -6 +/- 1 mmHg; cardiac output, 0.4 +/- 0.1 vs. 0.15 +/- 0.1 l/min). Bradykinin infusion led to dose-dependent decreases in mean aortic pressure and increases in cardiac output that were not modified by pretreatment with ciprokiren but were potentiated 10-fold by enalaprilat. Hoe-140 significantly reduced the hemodynamic effects of enalaprilat. Thus endogenous bradykinin is involved in the acute hemodynamic effects of enalaprilat in experimental heart failure.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8764248&dopt=Abstract
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