Exp Clin Endocrinol Diabetes 2006; 114 - P14_182
DOI: 10.1055/s-2006-933067

Native and oxidized LDL potentiate Endothelial cell mediated aldosterone secretion from the steroidogenic cells

I Ansurudeen 1, M Ehrhart-Bornstein 1, RS Bornstein 1, S Kopprasch 1
  • 1Carl Gustv Carus Medical school, Technical University, Dresden, Germany

Aldosterone secreted by the adrenal cortex maintains water and electrolyte balance and regulates blood pressure homeostasis. The aldosterone synthesizing zona glomerulosa of the adrenal cortex is a highly vascularized region. This allows complex interaction between the steroidogenic cells and the vascular endothelial cells, regulating the hormonal output. Steroidogenesis starts from cholesterol provided by the circulating LDL and HDL. Substantial interactions also occur between the circulating LDLs and the vascular endothelial cells. Previous studies show that endothelial cells positively regulate aldosterone levels. The role of native LDL (nLDL) and oxidized LDL (oLDL) on endothelial cell mediated aldosterone release would be clinically significant for hypertensive or atherosclerotic pathological conditions.

Objectives: The aim of the study was to investigate the effect of nLDL and oLDL on endothelial cell mediated aldosterone production.

Methods: The human vein endothelial cells (HUVEC) and human adrenocortical cells (NCI H295R) were cultured as per the protocol. HUVEC conditioned medium (HCM) was availed by treating HUVECs in serum free media for 24hrs with or without n/oLDL. The NCI cells were treated with HCM, nHCM, oHCM with or without inhibitors and measured for aldosterone levels.

Results: In this study, we show that stimulation of NCI with HCM over 24h increased the aldosterone production. This stimulation reached 70 to 80% of angiotensin II or forskolin induced stimulation of aldosterone secretion. A similar more pronounced effect was observed when NCI cells were stimulated with HCM from endothelial cells treated with nLDL (nHCM) or oLDL (oHCM). This enhanced aldosterone production was found to be more than an additive effect of n/oLDL and HCM. This increase was not affected by nitric oxide (NO), endothelin receptor (ET) or cyclooxygenase (COX) inhibitors.

Conclusion: Our results show that nHCM and oHCM can potentiate the aldosterone release from steroidogenic NCI cells and the factor involved in this effect is not NO, ET or COX substrates.