PuSH - Publikationsserver des Helmholtz Zentrums München: Increased aldosterone/renin quotient in obese hypertensive women: A novel role for low-density lipoproteins?

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Lamounier-Zepter, V.* ; Rotthoff, T.* ; Ansurudeen, I.* ; Kopprasch, S.* ; Scherbaum, W.A.* ; Ehrhart-Bornstein, M.* ; Bornstein, S.R.*

Increased aldosterone/renin quotient in obese hypertensive women: A novel role for low-density lipoproteins?

Horm. Metab. Res. 38, 471-475 (2006)

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Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.

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Obesity, especially visceral obesity, is strongly associated with arterial hypertension. Indeed, obesity hypertension has to be considered as the most common form of essential hypertension. However, the exact nature of the relationship between obesity and increased blood pressure remains poorly understood. Involvement of renin-independent mechanisms has been suggested in adrenal stimulation of aldosterone secretion in obese patients. This investigation examined the plasma levels of renin, aldosterone, insulin, and HDL and LDL in obese hypertensive and obese normotensive women. The group of hypertensive obese women showed significantly reduced plasma levels of renin and increased aldosterone/renin quotient (ARQ) compared to obese normotensive women. Plasma aldosterone levels were not significantly different between hypertensive and normotensive obese women. In addition, plasma levels of LDL-cholesterol in the hypertensive obese group were significantly increased in comparison to the obese normotensive group. No differences were observed in HDL-cholesterol or total cholesterol/HDL-C ratios between the two groups. We therefore examined the effect of LDL on angiotensin II-stimulated aldosterone release from human adrenocortical H295R cells. Treatment of adrenocortical cells with LDL led to a sensitization towards stimulation by angiotensin II, dramatically increasing angiotensin II-induced aldosterone production, so the increased aldosterone/renin ratio observed in the hypertensive group may be due to the enhanced LDL levels in these patients and/or other adipocyte-derived mineralocorticoid-stimulating factors.

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