Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function.
The ability of glucocorticoids to directly alter arterial function, structure and the inflammatory response to vascular injury may contribute to their well-established link with the development of cardiovascular disease. Recent studies have emphasised the importance of tissue-specific regulation of glucocorticoid availability by the 11 beta-hydroxysteroid dehydrogenase (11HSD) isozymes, which inter-convert active glucocorticoids and their inactive metabolites. The expression of both type 1 and type 2 11HSDs in the arterial wall suggests that prereceptor metabolism of glucocorticoids may have a direct impact on vascular physiology. Indeed there is evidence that 11HSDs influence glucocorticoid-mediated changes in vascular contractility, vascular structure, the inflammatory response to injury and the growth of new blood vessels. Hence, inhibition of 11HSD isozymes may provide a novel therapeutic target in vascular disease.
Hadoke
P W F
PW
Endocrinology Unit, Centre for Cardiovascular Science, Edinburgh University, The Queen's Medical Research Institute, 47, Little France Crescent, Edinburgh EH16 4TJ, Scotland (United Kingdom). phadoke@staffmail.ed.ac.uk
Macdonald
L
L
Logie
J J
JJ
Small
G R
GR
Dover
A R
AR
Walker
B R
BR
D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000502:physiology*; D000818:Animals; D001808:Blood Vessels / Q000737:chemistry / Q000254:growth & development* / Q000502:physiology*; D005938:Glucocorticoids / Q000032:analysis / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000209:etiology; D015398:Signal Transduction / Q000502:physiology
D005938:Glucocorticoids; D042842:11-beta-Hydroxysteroid Dehydrogenases