title: Effects of antihypertensive drugs and gene variants in the renin-angiotensin system.
abstract: Many genes and environmental factors are involved in the pathogenesis of hypertension, but the exact cause of essential hypertension has not yet been clarified. Gene polymorphism of the renin-angiotensin system (RAS) is one of the candidates. In the current study, we examined whether there was a correlation between the gene polymorphisms in RAS and either the choice of antihypertensive drugs or their efficacy. Subjects with essential hypertension (n=299) were recruited from among the outpatients of Osaka University Hospital and provided their informed consent for genetic analysis. Physicians freely chose the antihypertensive drugs and adjusted its dose until the patient's blood pressure was well controlled. The efficacy of each antihypertensive drug was estimated using the following formula: ABP=BP 1 (before treatment) - BP 2 (after treatment)/BP 1 x 100 (%). Gene variants in RAS were determined using PCR or PCR-RFLP (restriction fragment of polymorphism). The gene polymorphisms of RAS were not associated with delta SBP or ADBP. However, the mean ASBP in subjects with a deletion homozygote of the angiotensin converting enzyme gene (ACE/DD) was significantly lower (p<0.05) than that in patients with an insertion I allele of the ACE gene. The gene polymorphisms of RAS did not significantly affect the choice of antihypertensive drugs. Even though gene polymorphism in the renin angiotensin system was not a major factor in the antihypertensive therapy, the determination of genotype might be of help in the management of essential hypertension.
authors.affiliation: Department of Geriatric Medicine, Osaka University Graduate School of Medicine, Suita, Japan. tkatsuya@yo.rim.or.jp
authors.forename: T
authors.initials: T
authors.lastname: Katsuya
authors.forename: Y
authors.initials: Y
authors.lastname: Iwashima
authors.forename: K
authors.initials: K
authors.lastname: Sugimoto
authors.forename: M
authors.initials: M
authors.lastname: Motone
authors.forename: T
authors.initials: T
authors.lastname: Asai
authors.forename: M
authors.initials: M
authors.lastname: Fukuda
authors.forename: Y
authors.initials: Y
authors.lastname: Fu
authors.forename: Y
authors.initials: Y
authors.lastname: Hatanaka
authors.forename: M
authors.initials: M
authors.lastname: Ohishi
authors.forename: H
authors.initials: H
authors.lastname: Rakugi
authors.forename: J
authors.initials: J
authors.lastname: Higaki
authors.forename: T
authors.initials: T
authors.lastname: Ogihara
mesh_terms: D000959:Antihypertensive Agents / Q000627:therapeutic use*; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D014644:Genetic Variation; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000188:drug therapy* / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D011110:Polymorphism, Genetic; D012084:Renin-Angiotensin System / Q000235:genetics*; D016896:Treatment Outcome
chemical_list: D000959:Antihypertensive Agents