(Hypertension. 1998;32:1077-1082.)
© 1998 American Heart Association, Inc.
Scientific Contributions |
Renal 11ß-Hydroxysteroid Dehydrogenase in Genetically Salt-Sensitive Hypertensive Rats
From the Second Department of Internal Medicine (Y.T., S.I., K.F.) and Department of Health Sciences (Y.T.), School of Medicine, Kanazawa University, and Third Department of Internal Medicine, Fukui Medical School (I.M.), Japan.
Correspondence to Yoshiyu Takeda, MD, Second Department of Internal Medicine, School of Medicine, Kanazawa University, 13-1 Takara-machi, Kanazawa 920, Japan. E-mail takeday{at}mhs.mp.kanazawa-u.ac.jp
Abstract—Renal 11ß-hydroxysteroid dehydrogenase II (11ß-HSDII) converts glucocorticoids into inactive metabolites and plays an important role in controlling blood pressure and sodium retention. To examine whether this enzyme may be involved in the pathophysiology of salt-sensitive hypertension, we determined 11ß-HSDII activity and mRNA levels in the blood vessel and kidney of Dahl Iwai salt-sensitive (DS) rats and Dahl Iwai salt-resistant (DR) rats. Urinary free corticosterone:free 11-dehydrocorticosterone ratio was measured to estimate renal 11ß-HSD activity. Vascular 11ß-HSDII activity was expressed as percent conversion of [3H]corticosterone to [3H]11-dehydrocorticosterone in homogenized mesenteric arteries. 11ß-HSDII mRNA was estimated with the use of competitive polymerase chain reaction (PCR). Renal 11ß-HSDII activity and mRNA levels were significantly decreased in 8- and 12-week-old high salt DS rats compared with DR, Sprague-Dawley (SD), or low salt DS rats of the same age. Decreased 11ß-HSDII activity and mRNA levels in mesenteric arteries were observed in 8- and 12-week-old high salt DS rats. Urinary excretion of 11ß-HSDII inhibitory factors was measured by inhibition of enzyme activity in microsomes from human kidney. The urinary inhibitors were significantly increased in 8- and 12-week-old high salt DS rats compared with DR, SD, or low salt DS rats of the same age. There were no significant differences in 11ß-HSDII activity and mRNA levels in mesenteric arteries and kidney or in urinary inhibitors between 4-week-old DS, DR, and SD rats. These results indicate that 11ß-HSDII may play a role in salt sensitivity and development of hypertension in the DS rat.
Key Words: glucocorticoids • mineralocorticoids • rats, Dahl • kidney • hypertension, essential • sodium
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