Biochemical and genetic characterization of 11 beta- hydroxysteroid dehydrogenase type 2 in low-renin essential hypertensives

dc.contributor.authorCarvajal, CA
dc.contributor.authorRomero, DG
dc.contributor.authorMosso, LM
dc.contributor.authorGonzalez, AA
dc.contributor.authorCampino, C
dc.contributor.authorMontero, J
dc.contributor.authorFardella, CE
dc.date.accessioned2024-01-10T12:37:49Z
dc.date.available2024-01-10T12:37:49Z
dc.date.issued2005
dc.description.abstractBackground The 11beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2) catalyzes the conversion of cortisol M to cortisone (E), avoiding the interaction of cortisol with the mineralocorticoid receptor. If it fails, cortisol will stimulate sodium and water reabsorption, increasing the intravascular volume that suppresses renin and secondarily increase the blood pressure.
dc.description.abstractObjective To look for the possible contribution of a decreased ability of 11betaHSD2 to convert cortisol to its inactive metabolite cortisone in the pathogenesis of low renin hypertension (LREH).
dc.description.abstractPatients and methods We studied 64 LREH patients (plasma renin activity, PRA < 1 ng/ml per h), eighty normorenin essential hypertensives MEW (PRA: 1-2.5 ng/ml per h) and 74 normotensives. Serum aldosterone (SA), F, E and serum F/E ratio was determined in all patients. A serum F/E ratio was considered high when it was higher than X + 2SD from the normotensive value. Cytosine-adenine (CA)-repeat microsatellite region in intron 1 of HSD11B2 gene was genotyped in all patients and normotensives volunteers. In 13 LREH with high F/E ratio we performed HSD11B2 gene sequencing.
dc.description.abstractResults LREH had serum F/E ratio higher than NREH and normotensive controls (3.6 (2.9-4.3) versus 2.9 (2.2-4.3) versus 3.0 (2.4-3.7) (P = 0.004), respectively). We observed an inverse relation between F/E ratio and SA and PRA. In NREH and normotensives we did not find correlation between these variables. In the LREH subset the longer 155 bp CA-allele showed the highest serum F/E ratio. No mutations in coding region or short introns were found in LREH patients.
dc.description.abstractConclusion In this study we show that low-renin essential hypertensives had increased serum cortisol/cortisone ratios as compared with normotensive subjects. This suggest that some essential hypertensives, with suppressed renin activity, may have an impairment in the cortisol inactivation catalyzed by the enzyme 11betaHSD2, whose low activity in LREH patients could be associated with the length of CA-repeat microsatellite in intron 1 of the HSD11B2 gene. (C) 2005 Lippincott Williams Wilkins.
dc.fechaingreso.objetodigital2024-04-30
dc.format.extent7 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1097/00004872-200501000-00015
dc.identifier.eissn1473-5598
dc.identifier.issn0263-6352
dc.identifier.pubmedidMEDLINE:15643127
dc.identifier.urihttps://doi.org/10.1097/00004872-200501000-00015
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76929
dc.identifier.wosidWOS:000226497900015
dc.information.autorucMedicina;Campino M;S/I;99519
dc.information.autorucMedicina;Carvajal C;S/I;8586
dc.information.autorucMedicina;Fardella C;S/I;66235
dc.information.autorucMedicina;Montero J;S/I;98797
dc.information.autorucMedicina;Mosso L;S/I;88201
dc.issue.numero1
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final77
dc.pagina.inicio71
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.revistaJOURNAL OF HYPERTENSION
dc.rightsacceso restringido
dc.subject11 beta-hydroxysteroid dehydrogenase type cortisol
dc.subjectcortisone
dc.subjectlow-renin hypertension
dc.subjectmutation
dc.subjectpolymorphisms
dc.subject11-BETA-HYDROXYSTEROID DEHYDROGENASE
dc.subjectHSD11B2
dc.subjectMUTATIONS
dc.subjectDEFECTS
dc.subjectHYPERALDOSTERONISM
dc.subjectALDOSTERONISM
dc.subjectMETABOLISM
dc.subjectCORTISOL
dc.subjectSUBUNIT
dc.subjectISOZYME
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleBiochemical and genetic characterization of 11 beta- hydroxysteroid dehydrogenase type 2 in low-renin essential hypertensives
dc.typeartículo
dc.volumen23
sipa.codpersvinculados99519
sipa.codpersvinculados8586
sipa.codpersvinculados66235
sipa.codpersvinculados98797
sipa.codpersvinculados88201
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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