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Biomedical subjects

A Mimran

Publications and source records attributed to A Mimran.

257 records · Page 15Linked to original sources
PubMedDate not supplied

[I/D gene polymorphism of the angiotensin-converting enzyme and left ventricular hypertrophy. Response to converting enzyme inhibitors].

BACKGROUND: The present study was designed to assess whether the angiotensin-converting enzyme (ACE) gene I/D polymorphism influence the ACE inhibitors effect on the regression of left ventricular hypertrophy. METHODS: Sixty hypertensive subjects never treated by antihypertensive drugs, aged 46 +/- 11 years, were included in the study. Follow-up with ACE inhibitor treatment was 60 +/- 26 months. Genotypes for ACE I/D polymorphism (DD, ID or II) were determined by PCR. The left ventricular mass index (LVMI) was assessed by two-dimensional directed M-mode echocardiography. RESULTS: ACE genotype distribution was in agreement with the Hardy-Weinberg equilibrium: 21 patients had the DD genotype, 29 were ID, and 10 were II. At baseline, age, systolic arterial pressure and LVMI didn't differ on the basis of genotype. Body mass index was significantly higher in II than in ID and DD groups. Regression of LVMI with ACE inhibitor treatment was similar in the 3 genotypes (-8.9%, -0.6%, -12.1% in DD, ID and II groups respectively). In addition, decrease of systolic arterial pressure was identical in 3 groups. CONCLUSION: ACE gene I/D polymorphism seems not to influence regression of left ventricular hypertrophy by ACE inhibitors in essential hypertension.

Adult↗
PubMedDate not supplied

[Influence of angiotensin I on angiogenesis in vitro in the rat].

The regulation of angiogenesis involves complex interactions. The aim of our study was to assess the influence of angiotensin II (ANG II) on different vascular beds in rat. Aortic, renal and mesenteric rings from 10 male Sprague-Dawley rats were cultured using a three-dimensional culture system consisting of rat type I collagen lattice. We assessed the influence of different ANG II concentrations (10(-7) et 10(-9) mol/L) on these rings as well as the effect of AT1 blockade by losartan (10(-7 mol/L). ANG II inhibited angiogenesis at 10(-7) mol/L on renal artery. However, these was a angiogenic effect at 10(-9) mol/L on the mesenteric artery. Every time losartan prevented the effect of ANG II in any kind of vessel rings. No significant effect on ANG II was found on aortic rings but coadministration of losartan induced a dramatic decrease in the number of capillary sprouts. In conclusion, ANG II seems to be deeply involved in angiogenesis. However, its effect depends on the concentration of ANG II and the type of vessel. ANG II appears to be angiogenic on mesenteric arteries via an AT1 receptor effect and mostly anti-angiogenic on the renal arteries with possible involvement of AT2 receptors.

Angiotensin II↗
PubMedDate not supplied

[Renin-angiotensin system inhibition and cardiac and renal alteration induced by a high sodium diet in rat].

BACKGROUND: The present study was designed to assess the influence of losartan on cardiac hypertrophy and albuminuria associated with early high sodium feeding in rats and to compare it to an angiotensin-converting enzyme inhibitor, enalapril, effect. METHODS: Male Sprague-Dawley rats received a regular diet (0.8% NaCl, NS, n=7), or high sodium diet (8% NaCl, HS, n=21) from weaning for 8 weeks. After 4 weeks of diet, two HS groups were treated or not for 4 weeks with losartan or enalapril (30 and 10 mg/kg(-1) x day(-1) respectively, n=7 in each). Food and water consumption, body weight, urinary volume and urinary excretion of sodium, potassium and albumin were measured at the end of treatment as well as arterial pressure (anesthetized rats), heart and kidney weight. RESULTS: Eight weeks after weaning, heart weight index and albuminuria were significantly higher in HS control group when compared to the control NS group without change of arterial pressure. Treatment with losartan or enalapril had no effect either on arterial pressure or cardio-renal alterations.

Albuminuria↗