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Titolo:
VASCULAR ALDOSTERONE - BIOSYNTHESIS AND A LINK TO ANGIOTENSIN-II-INDUCED HYPERTROPHY OF VASCULAR SMOOTH-MUSCLE CELLS
Autore:
HATAKEYAMA H; MIYAMORI I; FUJITA T; TAKEDA Y; TAKEDA R; YAMAMOTO H;
Indirizzi:
KKR HOKURIKU HOSP,2-13-43 IZUMIGOAKA KANAZAWA ISHIKAWA 920 JAPAN KKR HOKURIKU HOSP KANAZAWA ISHIKAWA 920 JAPAN KANAZAWA UNIV,SCH MED,DEPT INTERNAL MED 2 KANAZAWA ISHIKAWA 920 JAPAN KANAZAWA UNIV,SCH MED,DEPT BIOCHEM KANAZAWA ISHIKAWA 920 JAPAN
Titolo Testata:
The Journal of biological chemistry
fascicolo: 39, volume: 269, anno: 1994,
pagine: 24316 - 24320
SICI:
0021-9258(1994)269:39<24316:VA-BAA>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
POLYMERASE CHAIN-REACTION; STEROID 11-BETA-HYDROXYLASE; MINERALOCORTICOID RECEPTOR; PROTEIN-SYNTHESIS; GENE-EXPRESSION; MESSENGER-RNA; DNA; BINDING; CLONING; TISSUES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
H. Hatakeyama et al., "VASCULAR ALDOSTERONE - BIOSYNTHESIS AND A LINK TO ANGIOTENSIN-II-INDUCED HYPERTROPHY OF VASCULAR SMOOTH-MUSCLE CELLS", The Journal of biological chemistry, 269(39), 1994, pp. 24316-24320

Abstract

Mineralocorticoids have been suggested to act on blood vessels, leading to increased vasoreactivity and peripheral resistance. However, thesite of their production has so far been believed to be only the adrenal cortex. Here, we show direct evidence that vascular cells per se are aldosteronogenic, possessing their own system that responds to the steroid. Using polymerase chain reaction after reverse transcription, the CYP11B2 mRNA encoding the key enzyme for the biosynthesis of aldosterone was detected in both endothelial cells and smooth muscle cells cultivated from human pulmonary artery. The aldosterone receptor (type1 mineralocorticoid receptor) gene was also found to be expressed in smooth muscle cells and, to a lesser extent, in endothelial cells. CYP11B2 gene expression in smooth muscle cells was stimulated by angiotensin II, the effector peptide of the renin-angiotensin system. Furthermore, the angiotensin II-induced increase in [H-3]leucine incorporationin smooth muscle cells was significantly enhanced by aldosterone but inhibited by ZK 91587, a type 1 mineralocorticoid receptor antagonist. This may indicate that vascular aldosterone participates in the angiotensin II-induced hypertrophy of vascular smooth muscle cells. The present study therefore provides the starting point for a novel understanding of the molecular basis of vascular remodeling and hypertension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 16:30:46