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Biomedical subjects

L Becú

Publications and source records attributed to L Becú.

11 recordsLinked to original sources
PubMed1989

[Sodium transport in red blood cell membranes in essential arterial hypertension].

Several abnormalities in Na metabolism have been implicated in the pathogenesis of essential hypertension. In addition, recent work by several investigators has showed that some Na transport systems in red cell membranes may be altered in those patients. In order to confirm such abnormalities we evaluated simultaneously four different and clearly defined Na transport systems in red cell membranes: the ouabain sensitive Na pump (P) and the Na-K cotransport (Co) in nystatin loaded cells, the maximal rate of Na-Li countertransport (CTT) in lithium loaded cells and the rate constant of Na passive permeability (pp) in 58 normotensive control subjects with no family history of hypertension (N), 19 normotensive subjects with family history of hypertension (NH) and 34 essential hypertensive patients (HE). The mean (mean +/- SEM microns/lc/h) value of the P and pp was found to be comparable in the three groups. Co was found significantly decreased in both HE (241 +/- 28) and in NH (227 +/- 42) when compared to the control group (290 +/- 10). Although NH also showed CTT values (377 +/- 87) higher than controls, the difference did not reach statistical significance. Our results indicate that approximately 90.9% of both HE and NH presented abnormalities in one or more of the various Na transport systems studied. Normotensive patients with a positive family history and alterations in some of the Na transport systems in red cell membranes may prove an interesting experimental model to assess the importance of such alterations for the development of hypertension.

Adolescent↗
PubMed1988

Long-term systemic hypertension in children after successful repair of coarctation of the aorta.

The mechanisms responsible for long-term hypertension in children after successful repair of coarctation of the aorta have not yet been determined. We measured plasma renin activity and aldosterone, adrenalin, and noradrenalin concentrations both under basal conditions and in response to standing and treadmill exercise in 24 normal normotensive children, 16 normotensive postcoarctectomy children, eight hypertensive postcoarctectomy children, and seven children with essential hypertension. Exercise-induced changes in plasma renin activity, aldosterone, adrenalin, and noradrenalin were comparable in the four groups in spite of a significantly greater increase in systolic blood pressure in the children with hypertension. In response to standing, the plasma concentration of noradrenalin increased significantly in normotensive but not in hypertensive children. Hyperresponse of blood pressure to exercise in hypertensive postcoarctectomy children and children with essential hypertension is not related to abnormalities in the sympathetic nervous system or the angiotensin-aldosterone axis. Hypertension could be related to primary baroreceptor alterations, to structural changes in the arterial wall, or both. Twenty percent of normotensive postcoarctectomy children had a blood pressure hyperresponse to exercise and an abnormal noradrenalin response to standing similar to that seen in the hypertensive children. Follow-up of children after coarctectomy may elucidate whether these two abnormalities are indicators of an increased risk of developing long-term recurrent hypertension.

Aldosterone↗
PubMed1977

Supravalvular mitral stenosis associated with ventricular septal defect.

We describe three patients with supravalvular mitral stenosis caused by a diaphragm located just above the mitral valve and associated with a ventricular septal defect. Two of our three patients also had an associated coarctation of the aorta. The physical signs, ECGs, chest roentgenograms, and cardiac catheterization data are described. Points helpful in the differential diagnosis of this malformation are emphasized. All three patients were treated successfully by surgery.

Adolescent↗