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Hypertension. 1996;27:197-201

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(Hypertension. 1996;27:197-201.)
© 1996 American Heart Association, Inc.


Articles

Endogenous Renal 11ß-Hydroxysteroid Dehydrogenase Inhibitory Factors in Patients With Low-Renin Essential Hypertension

Yoshiyu Takeda; Isamu Miyamori; Kazuhiro Iki; Satoru Inaba; Kenji Furukawa; Haruhiko Hatakeyama; Takashi Yoneda; Ryoyu Takeda

From the Second Department of Internal Medicine (Y.T., I.M., K.I., S.I., K.F., H.H., T.Y., R.T.) and Department of Health Sciences (Y.T.), School of Medicine, Kanazawa (Japan) University.

Correspondence to Yoshiyu Takeda, MD, Second Department of Internal Medicine, School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920, Japan.

Abstract 11ß-Hydroxysteroid dehydrogenase (11ß-HSD) modulates the access of corticosteroids to their receptors and is important in blood pressure control. The excretion of renal 11ß-HSD (ie, NAD+-dependent isoform) is thought to protect renal mineralocorticoid receptors from cortisol. To examine whether endogenous renal 11ß-HSD inhibitory factor(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 11ß-HSD inhibitors were measured by the inhibition of 11ß-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 11ß-HSD inhibitors but did not affect the ratio of urinary tetrahydrocortisol+allo-tetrahydrocortisol to tetrahydrocortisone. Endogenous renal 11ß-HSD inhibitory factors may contribute to the pathogenesis of low-renin essential hypertension by modulating the activity of 11ß-HSD. Sodium intake may directly or indirectly regulate the inhibitory factors.


Key Words: hydroxysteroid dehydrogenase • adrenal cortex hormones • renin • kidney




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