J L Elghozi, G Dagher, R P Garay, D Vasmant, F Girard, P Meyer
{"title":"A case of juvenile essential hypertension: implications of erythrocyte net Na+, K+ flux measurement.","authors":"J L Elghozi, G Dagher, R P Garay, D Vasmant, F Girard, P Meyer","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>In recent studies were reported an inherited membrane defect which is closely related to the development of essential hypertension. This abnormality consists of a functional deficiency in the Na+--K+ co-transport mechanism in erythrocytes of essential hypertensives and some normotensives born of hypertensive parents. Here we report a case of juvenile essential hypertension including familial erythrocyte Na+, K+ measurements. The 2-year-old boy had essential hypertension and bore the abnormality, with no compensatory activity of the Na+, K+ pump. The mother had developed hypertension during pregnancy. She also bore the erythrocyte abnormality as the net Na+/K+ flux ratio was reduced. One sister bore the same abnormality without hypertension but a complete analysis of Na+ extrusion mechanisms in this patient demonstrated a compensatory effect of the Na+, K+ pump activity. Other members of the family were normotensive without the flux abnormality. It appears therefore that erythrocyte flux measurements might be of diagnostic and genetic interest in juvenile hypertension.</p>","PeriodicalId":9217,"journal":{"name":"Biomedicine / [publiee pour l'A.A.I.C.I.G.]","volume":"35 1","pages":"4-6"},"PeriodicalIF":0.0000,"publicationDate":"1981-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Biomedicine / [publiee pour l'A.A.I.C.I.G.]","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
In recent studies were reported an inherited membrane defect which is closely related to the development of essential hypertension. This abnormality consists of a functional deficiency in the Na+--K+ co-transport mechanism in erythrocytes of essential hypertensives and some normotensives born of hypertensive parents. Here we report a case of juvenile essential hypertension including familial erythrocyte Na+, K+ measurements. The 2-year-old boy had essential hypertension and bore the abnormality, with no compensatory activity of the Na+, K+ pump. The mother had developed hypertension during pregnancy. She also bore the erythrocyte abnormality as the net Na+/K+ flux ratio was reduced. One sister bore the same abnormality without hypertension but a complete analysis of Na+ extrusion mechanisms in this patient demonstrated a compensatory effect of the Na+, K+ pump activity. Other members of the family were normotensive without the flux abnormality. It appears therefore that erythrocyte flux measurements might be of diagnostic and genetic interest in juvenile hypertension.