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Titolo:
Genetic analysis of aldosterone synthase in patients with idiopathic hyperaldosteronism
Autore:
Takeda, Y; Furukawa, K; Inaba, S; Miyamori, I; Mabuchi, H;
Indirizzi:
Kanazawa Univ, Sch Med, Dept Internal Med 2, Kanazawa, Ishikawa 920, JapanKanazawa Univ Kanazawa Ishikawa Japan 920 , Kanazawa, Ishikawa 920, Japan Kanazawa Univ, Sch Med, Dept Hlth Sci, Kanazawa, Ishikawa 920, Japan Kanazawa Univ Kanazawa Ishikawa Japan 920 , Kanazawa, Ishikawa 920, Japan Fukui Med Sch, Dept Internal Med 3, Fukui 91011, Japan Fukui Med Sch Fukui Japan 91011 Dept Internal Med 3, Fukui 91011, Japan
Titolo Testata:
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
fascicolo: 5, volume: 84, anno: 1999,
pagine: 1633 - 1637
SICI:
0021-972X(199905)84:5<1633:GAOASI>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUCOCORTICOID-SUPPRESSIBLE HYPERALDOSTERONISM; POLYMERASE-CHAIN-REACTION; LOW-RENIN HYPERTENSION; LEYDIG-CELL TUMOR; REMEDIABLE ALDOSTERONISM; CHIMERIC GENE; STEROID 21-HYDROXYLASE; CYP11B2 GENE; BIOSYNTHESIS; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Takeda, Y KanazawashikawaSch Med, Dept Internal Med 2, 13-1 Takara Machi, Kanazawa, I Kanazawa Univ 13-1 Takara Machi Kanazawa Ishikawa Japan 920 a, I
Citazione:
Y. Takeda et al., "Genetic analysis of aldosterone synthase in patients with idiopathic hyperaldosteronism", J CLIN END, 84(5), 1999, pp. 1633-1637

Abstract

Idiopathic hyperaldosteronism (IHA) is characterized by hypertension with excessive production of aldosterone, potassium loss, and suppression of therenin-angiotensin system. We compared activity of aldosterone synthase andexpression of CYP11B2 messenger RNA (mRNA) in mononuclear leukocytes (MNL)from patients with IHA. to findings in leukocytes from patients with aldosterone-producing adenoma and normal controls. Aldosterone synthase activitywas estimated from conversion of [C-14]deoxycorticosterone to [C-14]aldosterone. Levels of CYP11B2 mRNA were determined by competitive PCR. In the same subjects, we sought the chimeric CYP11B1/CYP11B2 that is candidate gene for glucocorticoid-remediable hyperaldosteronism. Southern blot analysis and a long PCR method were used to detect the chimeric gene. Direct sequencing of the CYP11B2 also was performed. No chimeric genes or mutations in the coding region of the CYP11B2 were found in genomic DNA from these patients. However, both aldosterone synthase activity and CYP11B2 mRNA expression were greater in mononuclear leukocytes of patients with IHA than those of patients with aldosterone-producing adenoma or controls. These results suggestthat regulatory factors of the CYP11B2 gene, e.g. unidentified aldosterone-stimulating substances or abnormalities in the promoter region of the CYP11B2 gene in patients with IHA resulting in oversecretion, may cause overexpression of mRNA of CYP11B2.

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Documento generato il 30/11/20 alle ore 16:55:41