Julie A. Maguire

VASCULAR LOCALIZATION OF THE 11β‐HYDROXYSTEROID DEHYDROGENASE TYPE II ENZYME

1. The enzyme 11β‐hydroxysteroid dehydrogenase type II (11βHSD2) confers specificity on the non‐specific mineralocorticoid receptor by converting cortisol to cortisone.

Fas-induced apoptosis is a feature of progressive diabetic nephropathy in transgenic (mRen-2)27 rats: Attenuation with renin-angiotensin blockade

Background and Aim:  Tubular atrophy is a major feature of most renal diseases and is closely associated with the loss of renal function. The present study sought to investigate whether Fas/FasL‐induced tubular epithelial cell apoptosis was a feature of experimental diabetic nephropathy. The effects of renoprotective therapy with blockade of the renin‐angiotensin (RAS) system were also examined.

Vascular localization of the 11 beta-hydroxysteroid dehydrogenase type II enzyme

1. The enzyme 11β‐hydroxysteroid dehydrogenase type II (11βHSD2) confers specificity on the non‐specific mineralocorticoid receptor by converting cortisol to cortisone.

VASCULAR LOCALIZATION OF THE 11?-HYDROXYSTEROID DEHYDROGENASE TYPE II ENZYME

1. The enzyme 11β‐hydroxysteroid dehydrogenase type II (11βHSD2) confers specificity on the non‐specific mineralocorticoid receptor by converting cortisol to cortisone.

11β hydroxysteroid dehydrogenase type 2 enzyme is expressed in normotensive and hypertensive patients with renal disease

SUMMARY: The enzyme 11β hydroxysteroid dehydrogenase type 2 (11βHSD2) converts glucocorticoids to their 11‐keto metabolites, permitting binding of aldosterone to the non‐selective mineralocorticoid receptor. Recent studies have suggested that 11βHSD deficiency may be implicated in essential hypertension and renal disease. Using an antibody against a peptide deduced from the cDNA sequence, the renal expression of 11βHSD2 was examined in patients with advanced stages of renal disease and associated hypertension, patients with primary hypertension resulting in renal damage, and patients with preserved or mildly damaged renal architecture without concomitant hypertension. Despite variable degrees of tubulointerstitial damage, 11βHSD2 was expressed in distal convoluted tubules and collecting ducts in all patient groups. Collapsed tubules retained strong immunoreactivity, but decreased staining was apparent in dilated tubules. There was weak staining of the thick ascending limb of Henle. Variable glomerular expression of 11βHSD2 was observed. Our results therefore suggest that absence of renal 11βHSD2 is not a prominent feature of hypertensive nephrosclerosis, or primary renal disease associated with hypertension.