European Heart Journal Advance Access originally published online on December 15, 2004
European Heart Journal 2005 26(5):498-504; doi:10.1093/eurheartj/ehi070
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
11ß-Hydroxysteroid dehydrogenase type 2 activity is associated with left ventricular mass in essential hypertension
1Hypertension and Cardiovascular Prevention Centre, ASL n.1-University of Sassari, Italy
2Emergency Department, ASL n.1, Sassari, Italy
3Hypertension Centre, University of Torino, Italy
Received 9 July 2004; revised 4 October 2004; accepted 28 October 2004; online publish-ahead-of-print 15 December 2004.
* Corresponding author. Tel:/fax: +39 079 228388. E-mail address: glorioso{at}uniss.it
Aims Left ventricular mass (LVM) is under the control of aldosterone and angiotensin II in experimental hypertension, but the effect of aldosterone on LVM is controversial in essential hypertension (EH). Some EH patients show a mild impairment of 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD2) activity without clinical features of the syndrome of apparent mineralocorticoid excess, where the incomplete cortisol-to-cortisone conversion leads to glucocorticoid-mediated mineralocorticoid effects. The mineralocorticoid receptor and 11ß-HSD2 are co-expressed in human heart. We investigated whether LVM may be regulated by glucocorticoids in EH patients.
Methods and results The ratio between 24 h urinary tetrahydro derivatives of cortisol and cortisone (THFs/THE), plasma renin activity, 24 h urinary aldosterone, blood pressure, and LVM indexed for height2.7 (LVMh2.7) were analysed in 493 never-treated hypertensives and 98 normotensives. THFs/THE was associated with LVMh2.7 in hypertensives and normotensives (r=0.32, P<0.001, and r=0.17, P=0.04, respectively) and persisted after adjusting for confounders (multiple regression analysis). Body mass index, sex, recumbent plasma renin activity, and THFs/THE accounted for 26.1% of LVMh2.7 variation. Urinary aldosterone was not correlated with LVMh2.7.
Conclusion We suggest that glucocorticoids may take part in the regulation of LVM in EH patients as a function of 11ß-HSD2 activity, and contribute to the target organ damage associated with essential hypertension.
Key Words: Cardiac mass • 11ß-Hydroxysteroid dehydrogenase • Mineralocorticoids • Glucocorticoids • Blood pressure
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  Wenxia Chai, Y. M Hoedemaekers, R. H. van Schaik, M. van Fessem, I. M Garrelds, J. J Saris, D. Dooijes, F. J ten Cate, M. M. Kofflard, and A. J. Danser Cardiac aldosterone in subjects with hypertrophic cardiomyopathy Journal of Renin-Angiotensin-Aldosterone System, December 1, 2006; 7(4): 225 - 230. [Abstract] [PDF]
|
|
|
|
 |
|
 S. A. Reini, C. E. Wood, E. Jensen, and M. Keller-Wood Increased maternal cortisol in late-gestation ewes decreases fetal cardiac expression of 11beta-HSD2 mRNA and the ratio of AT1 to AT2 receptor mRNA Am J Physiol Regulatory Integrative Comp Physiol, December 1, 2006; 291(6): R1708 - R1716. [Abstract] [Full Text] [PDF]
|
|