title: Renin angiotensin system blockage associates with insertion/deletion polymorphism of angiotensin-converting enzyme in patients with hypertensive emergency.
abstract: Hypertensive crisis (HC) stands out as a form of acute elevation of blood pressure (BP). It can manifest itself as hypertensive emergency (HE) or hypertensive urgency (HU), which is usually accompanied with levels of diastolic BP ≥120 mmHg. Angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism may influence manifestations of HC. Thus, this study evaluated the influence of ACE I/D polymorphism in individuals with HC. A total of 187 patients admitted with HC (HU [n=69] and HE [n=118]) and 75 normotensive individuals were included in the study. Peripheral blood was drawn for a biochemical and genetic analysis of the ACE I/D polymorphism by Polymerase Chain Reaction. HC group showed higher systolic BP, body mass index (BMI), glycemia, creatinine, and lower high-density lipoprotein (HDL) cholesterol compared with normotensive individuals. The use of renin-angiotensin system (RAS) blockers was more frequent in the HU group than in the HE group (p=0.020). The II genotype was more predominant in normotensive and HU individuals than among HE individuals (18.7%, 11.6%, and 2.5%, respectively; p=0.004). Higher BMI and glycemia were associated with HC in the logistic regression model. ACE II genotype (odds ratio [OR] 0.14; 95% confidence interval [CI] 0.04-0.51) and HDL cholesterol were protective for the development of HE. ACE II genotype was present in the HU group, compared with the HE group (OR 0.18; 95% CI 0.04-0.88). This study shows an association between the low prevalence of ACE I/D polymorphism II genotype and a greater occurrence of HE in Brazilian individuals. The lower blockage of RAS, which was detected in the HE group, may interact with the low frequency of II genotype, conferring an increased risk for HE.
authors.affiliation: Internal Medicine Department, Hypertension Clinic-Hospital de Base, State Medical School of São José do Rio Preto (FAMERP), São Paulo, Brazil. vilelamartin@uol.com.br
authors.forename: José F
authors.initials: JF
authors.lastname: Vilela-Martin
authors.forename: Renan O
authors.initials: RO
authors.lastname: Vaz-de-Melo
authors.forename: Luciana N
authors.initials: LN
authors.lastname: Cosenso-Martin
authors.forename: Cristina H
authors.initials: CH
authors.lastname: Kuniyoshi
authors.forename: Juan C
authors.initials: JC
authors.lastname: Yugar-Toledo
authors.forename: Marcela A S
authors.initials: MA
authors.lastname: Pinhel
authors.forename: Gisele F
authors.initials: GF
authors.lastname: de Souza
authors.forename: Dorotéia R S
authors.initials: DR
authors.lastname: Souza
authors.forename: Eduardo
authors.initials: E
authors.lastname: Pimenta
authors.forename: Heitor
authors.initials: H
authors.lastname: Moreno
authors.forename: José P
authors.initials: JP
authors.lastname: Cipullo
mesh_terms: D000328:Adult; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000959:Antihypertensive Agents / Q000494:pharmacology; D001794:Blood Pressure / Q000235:genetics; D015992:Body Mass Index; D001938:Brazil / Q000453:epidemiology; D016022:Case-Control Studies; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000453:epidemiology / Q000235:genetics*; D054643:INDEL Mutation; D008077:Lipoproteins, LDL / Q000097:blood; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics* / Q000378:metabolism; D011110:Polymorphism, Genetic; D015995:Prevalence; D012084:Renin-Angiotensin System / Q000187:drug effects*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D008077:Lipoproteins, LDL; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A