Abstract

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 height^2.7 (LVMh^2.7) were analysed in 493 never-treated hypertensives and 98 normotensives. THFs/THE was associated with LVMh^2.7 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 LVMh^2.7 variation. Urinary aldosterone was not correlated with LVMh^2.7. 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.

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