title: Pathophysiological roles of the adrenal renin-angiotensin system in patients with primary aldosteronism.
abstract: The mechanism of overproduction of aldosterone in primary aldosteronism is unclear. The intraadrenal renin-angiotensin system (RAS) has been suggested to possess the functional role of the synthesizing aldosterone and regulating blood pressure. In order to clarify the pathophysiological roles of adrenal RAS in aldosterone-producing adenoma (APA), we studied the expressions of the messenger RNAs (mRNAs) of renin, angiotensinogen, type 1 (AT1R) and type 2 angiotensin II receptor (AT2R), CYP11B1 (11 beta-hydroxylase gene) and CYP11B2 (aldosterone synthase gene) in 8 patients with angiotensin II-responsive (ATII-R) APA and compared them with the expressions of the same mRNAs in 8 patients with angiotensin II-unresponsive (ATII-U) APA. Quantification of the mRNA of each gene was done using a real-time polymerase chain reaction with specific primers. There were no significant differences between ATII-R APA and ATII-U APA in the mRNA levels of renin, angiotensinogen, AT1 R, CYP11B1 and CYP11B2. The amount of AT2R mRNA was significantly higher in the patients with ATII-R APA than in those with ATII-U APA (p<0.05). These results may suggest that AT2R partially contributes to the overproduction of aldosterone in ATII-R APA.
authors.affiliation: Molecular Genetics of Cardiovascular Disorders, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan. tennari0118@yahoo.co.jp
authors.forename: Nobushige
authors.initials: N
authors.lastname: Oda
authors.forename: Yoshiyu
authors.initials: Y
authors.lastname: Takeda
authors.forename: Aoshuang
authors.initials: A
authors.lastname: Zhu
authors.forename: Mikiya
authors.initials: M
authors.lastname: Usukura
authors.forename: Takashi
authors.initials: T
authors.lastname: Yoneda
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Takata
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Mabuchi
mesh_terms: D000311:Adrenal Glands / Q000503:physiopathology*; D000328:Adult; D000808:Angiotensinogen / Q000096:biosynthesis / Q000235:genetics; D015153:Blotting, Western; D019405:Cytochrome P-450 CYP11B2 / Q000096:biosynthesis / Q000235:genetics; D004232:Diuretics; D005260:Female; D005665:Furosemide; D006801:Humans; D006929:Hyperaldosteronism / Q000175:diagnosis / Q000503:physiopathology*; D006973:Hypertension / Q000175:diagnosis / Q000209:etiology; D008297:Male; D008875:Middle Aged; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D044140:Receptor, Angiotensin, Type 1 / Q000096:biosynthesis / Q000235:genetics; D011945:Receptors, Angiotensin / Q000096:biosynthesis / Q000235:genetics; D012083:Renin / Q000096:biosynthesis / Q000235:genetics; D012084:Renin-Angiotensin System / Q000502:physiology*; D013252:Steroid 11-beta-Hydroxylase / Q000096:biosynthesis / Q000235:genetics
chemical_list: D004232:Diuretics; D012333:RNA, Messenger; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D000808:Angiotensinogen; D005665:Furosemide; D019405:Cytochrome P-450 CYP11B2; D013252:Steroid 11-beta-Hydroxylase; D012083:Renin