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Titolo:
11 beta-Hydroxysteroid dehydrogenase in cultured human vascular cells - Possible role in the development of hypertension
Autore:
Hatakeyama, H; Inaba, S; Miyamori, I;
Indirizzi:
Fukui Med Univ, Dept Internal Med 3, Fukui 9101141, Japan Fukui Med Univ Fukui Japan 9101141 Internal Med 3, Fukui 9101141, Japan
Titolo Testata:
HYPERTENSION
fascicolo: 5, volume: 33, anno: 1999,
pagine: 1179 - 1184
SICI:
0194-911X(199905)33:5<1179:1BDICH>2.0.ZU;2-B
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANGIOTENSIN-II RECEPTORS; SMOOTH-MUSCLE CELLS; GENE-EXPRESSION; MINERALOCORTICOID RECEPTOR; CHROMOSOMAL LOCALIZATION; MESENTERIC-ARTERIES; TISSUE DISTRIBUTION; RATS; ALDOSTERONE; KIDNEY;
Keywords:
11 beta-hydroxysteroid dehydrogenase; receptors, angiotensin II; cortisol; vascular tone; hypertension, essential;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Hatakeyama, H FukuinMed Univ, Dept Internal Med 3, 23-1 Matsuoka Cho, Fukui 9101141, Japa Fukui Med Univ 23-1 Matsuoka Cho Fukui Japan 9101141 , Japa
Citazione:
H. Hatakeyama et al., "11 beta-Hydroxysteroid dehydrogenase in cultured human vascular cells - Possible role in the development of hypertension", HYPERTENSIO, 33(5), 1999, pp. 1179-1184

Abstract

11 beta-Hydroxysteroid dehydrogenases (11 beta-HSD) interconvert cortisol,the physiological glucocorticoid, and its inactive metabolite cortisone inhumans. The diminished dehydrogenase activity (cortisol to cortisone) has been demonstrated in patients with essential hypertension and in resistancevessels of genetically hypertensive rats. 11 beta-Hydroxysteroid dehydrogenase type 2 (11 beta-HSD2) catalyzes only 11 beta-dehydrogenation. However,a functional relationship between diminished vascular 11 beta-HSD2 activity and elevated blood pressure has been unclear, In this study we showed theexpression and enzyme activity of 11 beta-HSD2 and 11 beta-HSD type 1 (which is mainly oxoreductase, converting cortisone to cortisol) in human vascular smooth muscle cells. Glucocorticoids and mineralocorticoids increase vascular tone by upregulating the receptors of presser hormones such as angiotensin II. We found that physiological concentrations of cortisol-induced increase in angiotensin II binding were significantly enhanced by the inhibition of 11 beta-HSD2 activity with an antisense DNA complementary to 11 beta-HSD2 mRNA, and the enhancement was partially but significantly abolished by a selective aldosterone receptor antagonist. This may indicate that impaired 11 beta-HSD2 activity in vascular wall results in increased vascular tone by the contribution of cortisol, which acts as a mineralocorticoid. In congenital 11 beta-HSD deficiency and after administration of 11 beta-HSD inhibitors, suppression of 11 beta-HSD2 activity in the kidney has been believed to cause renal mineralocorticoid excess, resulting in sodium retentionand hypertension. In the present study we provide evidence for a mechanismthat could link impaired vascular 11 beta-HSD2 activity, increased vascular tone, and elevated blood pressure without invoking renal sodium retention.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 10:37:13