11 $beta;-hydroxysteroid-dehydrogenase type 2 gene analysis in hypertensive and normotensive subjects
نویسندگان
چکیده
منابع مشابه
Age-related changes in 11β-hydroxysteroid dehydrogenase type 2 activity in normotensive subjects.
BACKGROUND Impairment in 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2) activity results in inefficient inactivation of cortisol to cortisone, and it can trigger hypertension through activation of the mineralocorticoid receptor. Information about age-related changes in 11β-HSD2 activity and its physiological consequences is scarce. Our aim was to investigate whether 11β-HSD2 activity is age...
متن کاملGene expression of 11 beta-hydroxysteroid dehydrogenase in the mesenteric arteries of genetically hypertensive rats.
11 beta-Hydroxysteroid dehydrogenase (11 beta-HSD) modulates the access of corticosteroids to their receptors and plays an important role in controlling blood pressure. We determined 11 beta-HSD activity and mRNA levels in the mesenteric arteries of genetically hypertensive rats, the Dahl salt-sensitive hypertensive rat, and compared them with Dahl salt-resistant and Sprague-Dawley rats. 11 bet...
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Cadmium, a common environmental pollutant and a major constituent of tobacco smoke, has been identified as a new class of endocrine disruptors with a wide range of detrimental effects on mammalian reproduction. During human pregnancy, maternal cadmium exposure, via the environment and/or cigarette smoking, leads to fetal growth restriction (FGR), but the underlying mechanisms are unknown. Altho...
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The enzyme 11-beta hydroxysteroid dehydrogenase type 2 plays a major role in blood pressure regulation. It metabolizes glucocorticoid hormones into derivatives with low affinity for the mineralocorticoid receptor, preventing its permanent occupancy by circulating cortisol, which is 100- to 1000-fold more abundant than aldosterone in the plasma. Inactivating mutations of the enzyme result in sev...
متن کاملPlacental 11 -Hydroxysteroid Dehydrogenase in Dahl and Spontaneously Hypertensive Rats
Studies in normotensive rats showed that excessive fetal exposure to maternal glucocorticoids retards growth and programs hypertension in later life. This excessive exposure is proposed to occur due to a reduction of the placental barrier to maternal glucocorticoids that is provided by 11 -hydroxysteroid dehydrogenase (11 HSD). To assess the possible alterations of glucocorticoid placental barr...
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ژورنال
عنوان ژورنال: American Journal of Hypertension
سال: 2003
ISSN: 0895-7061
DOI: 10.1016/s0895-7061(03)00282-6