PMID- 10824333
OWN - NLM
STAT- MEDLINE
DCOM- 20000606
LR  - 20131121
IS  - 0967-4845 (Print)
IS  - 0967-4845 (Linking)
VI  - 56
IP  - 3
DP  - 1999
TI  - 11 beta-Hydroxysteroid dehydrogenase: a link between the dysregulation of 
      cortisol metabolism and hypertension.
PG  - 215-25
AB  - Endocrine pathology is a well-recognised and important cause of human 
      hypertension. Recent research has highlighted the role of 11 beta-hydroxysteroid 
      dehydrogenase (11 beta-HSD) in the development of certain forms of hypertension. 
      This enzyme, which exists as two genetically unique isoforms, 11 beta-HSD1 and 11 
      beta-HSD2, is responsible for the interconversion of biologically active cortisol 
      with its inactive 11-oxo derivative, cortisone. Congenital deficiency of 11 
      beta-HDS2 results in inappropriate activation of the renal mineralocorticoid 
      receptor by cortisol, leading to hypertension, hypokalaemia and metabolic 
      alkalosis. Several authors have postulated a link between changes in 11 beta-HSD 
      activity and the development of certain forms of essential hypertension. The 
      existence of endogenous inhibitors of the enzyme provides compelling evidence in 
      favour of this hypothesis, but few have been able to demonstrate a clear link 
      between inhibition of 11 beta-HSD2 activity and hypertension by this mechanism. 
      Similarly, several authors have suggested a relationship between reduced 
      placental 11 beta-HSD2 activity, low birth weight with high placental weight, and 
      the development of hypertension in adulthood. However, no clear evidence to 
      suggest a direct correlation between birth weight, placental weight and 11 
      beta-HSD2 activity has been demonstrated. While the role of 11 beta-HSD in the 
      development of hypertension remains controversial, an understanding of the 
      interplay of this enzyme with both mineralocorticoid and glucocorticoid receptors 
      undoubtedly will yield data that will clarify this complex field.
FAU - Donovan, S J
AU  - Donovan SJ
AD  - School of Pharmacy and Biomedical Sciences, University of Portsmouth, England, 
      UK.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - Switzerland
TA  - Br J Biomed Sci
JT  - British journal of biomedical science
JID - 9309208
RN  - 0 (Receptors, Glucocorticoid)
RN  - 0 (Receptors, Mineralocorticoid)
RN  - EC 1.1.- (Hydroxysteroid Dehydrogenases)
RN  - EC 1.1.1.146 (11-beta-Hydroxysteroid Dehydrogenases)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - 11-beta-Hydroxysteroid Dehydrogenases
MH  - Humans
MH  - Hydrocortisone/*metabolism
MH  - Hydroxysteroid Dehydrogenases/*physiology
MH  - Hypertension/*enzymology/metabolism
MH  - Receptors, Glucocorticoid/physiology
MH  - Receptors, Mineralocorticoid/physiology
RF  - 149
EDAT- 2000/05/29 09:00
MHDA- 2000/06/10 09:00
CRDT- 2000/05/29 09:00
PHST- 2000/05/29 09:00 [pubmed]
PHST- 2000/06/10 09:00 [medline]
PHST- 2000/05/29 09:00 [entrez]
PST - ppublish
SO  - Br J Biomed Sci. 1999;56(3):215-25.