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Titolo:
ENDOGENOUS RENAL 11-BETA-HYDROXYSTEROID DEHYDROGENASE INHIBITORY FACTORS IN PATIENTS WITH LOW-RENIN ESSENTIAL-HYPERTENSION
Autore:
TAKEDA Y; MIYAMORI I; IKI K; INABA S; FURUKAWA K; HATAKEYAMA H; YONEDA T; TAKEDA R;
Indirizzi:
KANAZAWA UNIV,SCH MED,DEPT INTERNAL MED 2,13-1 TAKARA MACHI KANAZAWA ISHIKAWA 920 JAPAN KANAZAWA UNIV,SCH MED,DEPT HLTH SCI KANAZAWA ISHIKAWA 920 JAPAN
Titolo Testata:
Hypertension
fascicolo: 2, volume: 27, anno: 1996,
pagine: 197 - 201
SICI:
0194-911X(1996)27:2<197:ER1DIF>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
MINERALOCORTICOID ACTIVITY; ANGIOTENSIN SYSTEM; URINARY-EXCRETION; RATS; 19-NORALDOSTERONE; METABOLISM; LIQUORICE; CORTISOL; EXCESS; SODIUM;
Keywords:
HYDROXYSTEROID DEHYDROGENASE; ADRENAL CORTEX HORMONES; RENIN; KIDNEY;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
34
Recensione:
Indirizzi per estratti:
Citazione:
Y. Takeda et al., "ENDOGENOUS RENAL 11-BETA-HYDROXYSTEROID DEHYDROGENASE INHIBITORY FACTORS IN PATIENTS WITH LOW-RENIN ESSENTIAL-HYPERTENSION", Hypertension, 27(2), 1996, pp. 197-201

Abstract

11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD) modulates the access of corticosteroids to their receptors and is important in blood pressure control. The excretion of renal 11 beta-HSD tie, NAD(+)-dependent isoform) is thought to protect renal mineralocorticoid receptors from cortisol. To examine whether endogenous renal 11 beta-HSD inhibitoryfactor(s) may be involved in the pathophysiology of hypertension, we studied the urinary excretion of such inhibitors in 30 patients with low-renin essential hypertension and 20 normotensive control subjects. The effect of sodium restriction on the urinary excretion of the inhibitors was also evaluated in six normotensive control subjects. Urine was extracted with Sep-Pak cartridges and high-performance liquid chromatography. Endogenous renal 11 beta-HSD inhibitors were measured by the inhibition of 11 beta-HSD bioactivity in microsomes from the human kidney. The urinary excretion of the inhibitors was significantly increased in patients with low-renin essential hypertension (1280+/-88 nmol/d, mean+/-SEM) compared with normotensive control subjects (704+/-56 nmol/d) (P<.05). Ratios of urinary tetrahydrocortisol+allo-tetrahydrocortisol to tetrahydrocortisone did not differ significantly. Sodium restriction reduced the urinary excretion of the endogenous renal 11 beta-HSD inhibitors but did not affect the ratio of urinary tetrahydrocortisol+allo-tetrahydrocortisol to tetrahydrocortisone. Endogenous renal11 beta-HSD inhibitory factors may contribute to the pathogenesis of low-renin essential hypertension by modulating the activity of 11 beta-HSD. Sodium intake may directly or indirectly regulate the inhibitoryfactors.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 01/12/20 alle ore 10:34:25