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Titolo:
Functional adrenocorticotropic hormone receptor in cultured human vascularendothelial cells - Possible role in control of blood pressure
Autore:
Hatakeyama, H; Inaba, S; Taniguchi, N; Miyamori, I;
Indirizzi:
Fukui Med Univ, Dept Internal Med 3, Fukui 9101193, Japan Fukui Med Univ Fukui Japan 9101193 Internal Med 3, Fukui 9101193, Japan
Titolo Testata:
HYPERTENSION
fascicolo: 5, volume: 36, anno: 2000,
pagine: 862 - 865
SICI:
0194-911X(200011)36:5<862:FAHRIC>2.0.ZU;2-M
Fonte:
ISI
Lingua:
ENG
Soggetto:
11-BETA-HYDROXYSTEROID DEHYDROGENASE; INDUCED HYPERTENSION; LOCALIZATION; GLUCOCORTICOIDS; EXPRESSION; INHIBITION; ISOFORMS; GENE; ACTH;
Keywords:
adrenocorticotropic hormone; gene expression; gene regulation; hormones; hypertension, essential;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
22
Recensione:
Indirizzi per estratti:
Indirizzo: Hatakeyama, H Fukui Med Univ, Dept Internal Med 3, 23-1 Matsuoka Cho, Fukui 9101193, Japan Fukui Med Univ 23-1 Matsuoka Cho Fukui Japan 9101193 Japan
Citazione:
H. Hatakeyama et al., "Functional adrenocorticotropic hormone receptor in cultured human vascularendothelial cells - Possible role in control of blood pressure", HYPERTENSIO, 36(5), 2000, pp. 862-865

Abstract

Hypertension is a prominent feature of patients with Gushing's disease andectopic adrenocorticotropic hormone (ACTH) syndrome, who have elevated ACTH levels. Chronic administration of ACTH (1-24) also raises blood pressure in humans. This effect has been postulated to be due to AGTH-induced increases in cortisol secretion in the adrenal gland. It is well known that cortisol increases vascular tone by potentiating the vasoconstrictor action of anumber of presser hormones. In the present study, we show direct evidence that human aortic endothelial cells possess the ACTH receptor. Il P-Dehydrogenation, converting cortisol to its inactive metabolite, cortisone, mediated by vascular 11 beta -hydroxysteroid dehydrogenase type 2 is essential for the control of vascular tone, and the reduced activity may be relevant tothe pathogenesis of hypertension. We found that ACTH (1-24) dose-dependently decreased the gene expression and enzyme activity of 11 beta -hydroxysteroid dehydrogenase type 2 in these cells, and the decrease was partially abolished by a selective ACTH receptor antagonist. This may indicate that ACTH potentiates the action of cortisol through its direct effect on the vasculature. Therefore, the present study provides important information for understanding the mechanism of ACTH-induced hypertension.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/11/20 alle ore 16:46:43