Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico

Background: Cortisol has been implicated in hypertension and lately reported to be regulated at the pre-receptor level by the 11ßHSD1 enzyme, which converts cortisone (E) to cortisol (F). Over expression ofthis enzyme in adipose tissue could determine an increase in available cortisol that interacts...

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Autores principales:	Morales,Mauricio A, Carvajal,Cristian A, Ortiz,Eugenia, Mosso,Lorena M, Artigas,Rocío A, Owen,Gareth I, Fardella,Carlos E
Lenguaje:	Spanish / Castilian
Publicado:	Sociedad Médica de Santiago 2008
Materias:	11-beta-Hydroxysteroid dehydrogenase type 1 Hypertension Polymorphism, genetic
Acceso en línea:	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872008000600003
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spelling	oai:scielo:S0034-988720080006000032008-08-27Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénicoMorales,Mauricio ACarvajal,Cristian AOrtiz,EugeniaMosso,Lorena MArtigas,Rocío AOwen,Gareth IFardella,Carlos E 11-beta-Hydroxysteroid dehydrogenase type 1 Hypertension Polymorphism, genetic Background: Cortisol has been implicated in hypertension and lately reported to be regulated at the pre-receptor level by the 11ßHSD1 enzyme, which converts cortisone (E) to cortisol (F). Over expression ofthis enzyme in adipose tissue could determine an increase in available cortisol that interacts with the mineralocorticoid receptor (MR) in renal, brain and heart tissue, leading to similar hypertensive effects as in 11ßHSD2 impaired patients. Severa! polymorphisms have been reported in HSDl IB 1 gene (CAI5, CAI9 and InsA83557), which could modify HSDl IB 1 gene expression or activity. Aun: To determine the distribution and prevalence of CAI5, CAI9 and InsA83557 in the HSDl IBl gene, and to correlate these results with biochemical parameters in cortisol/ ACTH (HPA) and renin-angiotensin-aldosterone (RAA) axis in patients with essential hypertension (EH). Patients and Methods: We studied 113 EHpatients (76 non-obese and 37 obese, with a body mass índex >30 kg/m²) and 30 normotensive adults (NT). In each patient, we measured serum levéis of E E, serum aldosterone (SA), plasma renin activity (PRA), adrenocorticotrophic hormone (ACTH), the urinary free cortisol/creatinine (UFF/Cr), F/ACTH and SA/PRA ratios. Each polymorphism was studied by PCR and 8% polyacrylamide gel electrophoresis. Statistical associations were evaluated by Pearson correlations and the genetic equilibñum by the Hardy-Weinberg (H-W) equation. Results: We found all three polymorphisms in the EH and the NT group, both in genetic equilibñum. In obese essential hypertensives, the CAI5polymorphism showed association with SA/PRA ratio (r =0.189, p =0.012) and F/ACTH (r =0.301, p 0.048); CA19 also showed correlation with F/ACTH in obese EH (r = 0.220, p 0.009). The InsA83557polymorphism correlated with UFF/Cr in both EH (r =0.206; p =0.03), and in obese EH (r =0.354; p =0.05). Conclusions: The CAI5 and CAI9 polymorphism correlated with changes in biochemical parameters in HPA and RAA axis of obese essential hypertensives. These changes mayresult of modifications in the expression of 11ßHSD1, leading to increased cortisol and aldosterone levéis independent of ACTH and renin control, respectivelyinfo:eu-repo/semantics/openAccessSociedad Médica de SantiagoRevista médica de Chile v.136 n.6 20082008-06-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872008000600003es10.4067/S0034-98872008000600003
institution	Scielo Chile
collection	Scielo Chile
language	Spanish / Castilian
topic	11-beta-Hydroxysteroid dehydrogenase type 1 Hypertension Polymorphism, genetic
spellingShingle	11-beta-Hydroxysteroid dehydrogenase type 1 Hypertension Polymorphism, genetic Morales,Mauricio A Carvajal,Cristian A Ortiz,Eugenia Mosso,Lorena M Artigas,Rocío A Owen,Gareth I Fardella,Carlos E Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
description	Background: Cortisol has been implicated in hypertension and lately reported to be regulated at the pre-receptor level by the 11ßHSD1 enzyme, which converts cortisone (E) to cortisol (F). Over expression ofthis enzyme in adipose tissue could determine an increase in available cortisol that interacts with the mineralocorticoid receptor (MR) in renal, brain and heart tissue, leading to similar hypertensive effects as in 11ßHSD2 impaired patients. Severa! polymorphisms have been reported in HSDl IB 1 gene (CAI5, CAI9 and InsA83557), which could modify HSDl IB 1 gene expression or activity. Aun: To determine the distribution and prevalence of CAI5, CAI9 and InsA83557 in the HSDl IBl gene, and to correlate these results with biochemical parameters in cortisol/ ACTH (HPA) and renin-angiotensin-aldosterone (RAA) axis in patients with essential hypertension (EH). Patients and Methods: We studied 113 EHpatients (76 non-obese and 37 obese, with a body mass índex >30 kg/m²) and 30 normotensive adults (NT). In each patient, we measured serum levéis of E E, serum aldosterone (SA), plasma renin activity (PRA), adrenocorticotrophic hormone (ACTH), the urinary free cortisol/creatinine (UFF/Cr), F/ACTH and SA/PRA ratios. Each polymorphism was studied by PCR and 8% polyacrylamide gel electrophoresis. Statistical associations were evaluated by Pearson correlations and the genetic equilibñum by the Hardy-Weinberg (H-W) equation. Results: We found all three polymorphisms in the EH and the NT group, both in genetic equilibñum. In obese essential hypertensives, the CAI5polymorphism showed association with SA/PRA ratio (r =0.189, p =0.012) and F/ACTH (r =0.301, p 0.048); CA19 also showed correlation with F/ACTH in obese EH (r = 0.220, p 0.009). The InsA83557polymorphism correlated with UFF/Cr in both EH (r =0.206; p =0.03), and in obese EH (r =0.354; p =0.05). Conclusions: The CAI5 and CAI9 polymorphism correlated with changes in biochemical parameters in HPA and RAA axis of obese essential hypertensives. These changes mayresult of modifications in the expression of 11ßHSD1, leading to increased cortisol and aldosterone levéis independent of ACTH and renin control, respectively
author	Morales,Mauricio A Carvajal,Cristian A Ortiz,Eugenia Mosso,Lorena M Artigas,Rocío A Owen,Gareth I Fardella,Carlos E
author_facet	Morales,Mauricio A Carvajal,Cristian A Ortiz,Eugenia Mosso,Lorena M Artigas,Rocío A Owen,Gareth I Fardella,Carlos E
author_sort	Morales,Mauricio A
title	Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
title_short	Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
title_full	Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
title_fullStr	Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
title_full_unstemmed	Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico
title_sort	regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßhsd1) en hipertensión arterial esencial: posible rol etiopatogénico
publisher	Sociedad Médica de Santiago
publishDate	2008
url	http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872008000600003
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Regiones polimórficas del gen 11ß-hidroxiesteroide deshidrogenasa tipo 1 (11ßHSD1) en hipertensión arterial esencial: Posible rol etiopatogénico

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