Uninephrectomy reduces 11b-hydroxysteroid dehydrogenase type 1 in

lspit for 6 days in week 5 after UNX. The mRNA of 11b-Hsd1 indicating reduced 11b-HSD2 activity and enhanced access underlying arterial hypertension after UNX are poorly after UNX, suggesting a renal mechanism for this type of Draper & Stewart 2005). 11b-HSD1 is strongly expressed in collecting duct where it catalyzes the reaction of cortisol into 373Journal of Endocrinology (2012) 214, 373–380hypertension. Interestingly, Mimran et al. (1993) reported a decline in plasma renin activity in individuals with an increase cortisone and by this mechanism protects the mineralo-corticoid receptor (MR) from promiscuous activation by DOI: 10.1530/JOE-12-0200understood and investigations trying to identify these mechanisms after UNX are scarce. Talseth et al. (1986) observed a correlation between the decrease in glomerular filtration rate (GFR) and the increment in arterial pressure liver tissue and converts inactive cortisone into active cortisol. Overexpression of 11b-HSD1 in the liver induced hyper-tension by an unknown mechanism (Paterson et al. 2004). 11b-HSD2 on the contrary is expressed in the renal cortical5 mmHg over 5–10 years beyond that associated with normal aging and an increased risk for hypertension (Boudville et al. 2006, Davis 2009, Ibrahim et al. 2009). The mechanisms Cellular cortisol availability is modulated by the two 11b-hydroxysteroid dehydrogenase enzymes, 11b-HSD1 and 11b-HSD2 (Lakshmi & Monder 1988, Albiston et al. 1994,RT-PCR and the 11b-HSD activities were directly quantified in their corresponding tissues by determining the ratios of (tetrahydrocorticosteroneC5a-tetrahydrocorticosterone)