scholarly journals Lack of Association of the 11β-Hydroxysteroid Dehydrogenase Type 1 Gene 83,557insA and Hexose-6-Phosphate Dehydrogenase Gene R453Q Polymorphisms with Body Composition, Adrenal Androgen Production, Blood Pressure, Glucose Metabolism, and Dementia

2007 ◽  
Vol 92 (1) ◽  
pp. 359-362 ◽  
Author(s):  
Pauline Smit ◽  
Marieke J. H. J. Dekker ◽  
Frank Jan de Jong ◽  
Annewieke W. van den Beld ◽  
Jan W. Koper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Composition ◽  
Glucose Metabolism ◽  
Hydroxysteroid Dehydrogenase ◽  
Adrenal Androgen ◽  
Dehydrogenase Gene

scholarly journals Renal medullary 11β-hydroxysteroid dehydrogenase type 1 in Dahl salt-sensitive hypertension

2008 ◽  
Vol 36 (1) ◽  
pp. 52-58 ◽  
Author(s):  
Yong Liu ◽  
Ravinder J. Singh ◽  
Kristie Usa ◽  
Brian C. Netzel ◽  
Mingyu Liang
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Molecular Mechanisms ◽  
Renal Medulla ◽  
Hydroxysteroid Dehydrogenase ◽  
Induced Hypertension ◽  
Intensive Investigation ◽  
Salt Sensitive Hypertension ◽  
Interfering Rna

The Dahl salt-sensitive rat is a widely used model of human salt-sensitive forms of hypertension. The kidney plays an important role in the pathogenesis of Dahl salt-sensitive hypertension, but the molecular mechanisms involved remain a subject of intensive investigation. Gene expression profiling studies suggested that 11β-hydroxysteroid dehydrogenase type 1 might be dysregulated in the renal medulla of Dahl salt-sensitive rats. Additional analysis confirmed that renal medullary expression of 11β-hydroxysteroid dehydrogenase type 1 was downregulated by a high-salt diet in SS-13BN rats, a consomic rat strain with reduced blood pressure salt sensitivity, but not in Dahl salt-sensitive rats. 11β-Hydroxysteroid dehydrogenase type 1 is known to convert inactive 11-dehydrocorticosterone to active corticosterone. The urinary corticosterone/11-dehydrocorticosterone ratio as well as urinary excretion of corticosterone was higher in Dahl salt-sensitive rats than in SS-13BN rats. Knockdown of renal medullary 11β-hydroxysteroid dehydrogenase type 1 with small-interfering RNA attenuated the early phase of salt-induced hypertension in Dahl salt-sensitive rats and reduced urinary excretion of corticosterone. Knockdown of 11β-hydroxysteroid dehydrogenase type 1 did not affect blood pressure in SS-13BN rats. Long-term attenuation of salt-induced hypertension was achieved with small hairpin RNA targeting renal medullary 11β-hydroxysteroid dehydrogenase type 1. In summary, we have demonstrated that suppression of 11β-hydroxysteroid dehydrogenase type 1 expression in the renal medulla attenuates salt-induced hypertension in Dahl salt-sensitive rats.

scholarly journals Uninephrectomy reduces 11β-hydroxysteroid dehydrogenase type 1 and type 2 concomitantly with an increase in blood pressure in rats

2012 ◽  
Vol 214 (3) ◽  
pp. 373-380 ◽  
Author(s):  
M Lauterburg ◽  
G Escher ◽  
B Dick ◽  
D Ackermann ◽  
F J Frey
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Hydroxysteroid Dehydrogenase ◽  
Gas Chromatography Mass Spectrometry ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Arterial Blood

Renal allograft donors are at risk of developing hypertension. Here, we hypothesized that this risk is at least in part explained by an enhanced intracellular availability of 11β-hydroxyglucocorticoids due to an increased 11β-hydroxysteroid dehydrogenase type 1 enzyme (11β-HSD1), an intracellular prereceptor activator of biologically inactive 11-ketocorticosteroids in the liver, and/or a diminished 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), an inactivator of 11β-hydroxyglucocorticoids in the kidney. To test this hypothesis, uninephrectomized (UNX) (n=9) and sham-operated (n=10) adult Sprague–Dawley rats were investigated. Mean arterial blood pressure and heart rate were measured continuously by telemetry for 6 days in week 5 after UNX. The mRNA of11β-Hsd1and11β-Hsd2in liver and kidney tissues were assessed by RT-PCR and the 11β-HSD activities were directly quantified in their corresponding tissues by determining the ratios of (tetrahydrocorticosterone+5α-tetrahydrocorticosterone)/tetrahydrodehydrocorticosterone ((THB+5α-THB)/THA) and of corticosterone/dehydrocorticosterone (B/A) by gas chromatography–mass spectrometry. The apparent total body activities of 11β-HSD1 and 11β-HSD2 were estimated using the urinary and plasma ratios of (THB+5α-THB)/THA and B/A. Mean arterial blood pressure was increased after UNX when compared with sham operation. Hepatic mRNA content of11β-Hsd1and hepatic, plasma, and urinary ratios of (THB+5α-THB)/THA were decreased after UNX, indicating diminished access of glucocorticoids to its receptors. In renal tissue,11β-Hsd2mRNA was reduced and B/A ratios measured in kidney, plasma, and urine were increased, indicating reduced 11β-HSD2 activity and enhanced access of glucocorticoids to mineralocorticoid receptors. Both 11β-HSD1 and 11β-HSD2 are downregulated after UNX in rats, a constellation considered to induce hypertension.

scholarly journals Synthesis and theoretical activity of three steroid-derivatives on both aromatase and 17β-hydroxysteroid dehydrogenase Type 1 enzymes

2019 ◽  
Vol 9 (2) ◽  
pp. 3898-3906
Keyword(s):  
Breast Cancer ◽  
Blood Pressure ◽  
Bone Loss ◽  
Hydroxysteroid Dehydrogenase ◽  
Secondary Effects ◽  
Cancer Breast ◽  
Docking Model ◽  
Common Malignancy

Breast cancer is the most common malignancy in the worldwide. It is noteworthy, that several drugs are used for cancer breast; nevertheless, some these drugs can produce secondary effects such as changes in blood pressure, bone loss and others. The objective of this investigation was synthesizing three steroid derivatives (compounds 4, 5 and 6) to evaluate their theoretical activity against both aromatase (2W3D) and 17β-Hydroxysteroid dehydrogenase Type 1 (3BH4) enzymes using fisetin and exemestane as control in a docking model. The data found indicate that compound 5 could exert a greater interaction with the 2WD4 and 3BH4 proteins in comparison with fisetin, exemestane and compounds 4 or 6. In conclusion, this compound could be a good candidate as both aromatase and 17β-hydroxysteroid dehydrogenase enzymes inhibitor.

LACK OF MUTATIONS OF TYPE 1 11β-HYDROXYSTEROID DEHYDROGENASE GENE IN PATIENTS WITH ABDOMINAL OBESITY

2001 ◽  
Vol 27 (1-2) ◽  
pp. 47-61 ◽  
Author(s):  
Elisabetta Caramelli ◽  
Pierluigi Strippoli ◽  
Tiziana Di Giacomi ◽  
Catleen Tietz ◽  
Paolo Carinci ◽  
...  
Keyword(s):  
Abdominal Obesity ◽  
Hydroxysteroid Dehydrogenase ◽  
Dehydrogenase Gene
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