The outer cells of the adrenal cortex help regulate blood pressure through the production of aldosterone. The renin/angiotensin II/ aldosterone system (RAAS) tightly regulates this production. Two regulatory steps are important in limiting the process; the expression and activity of the steroidogenic acute regulatory (StAR) protein, and the conversion of deoxycorticosterone to aldosterone in the mitochondria by aldosterone synthase (CYP11B2). Very low-density lipoproteins (VLDL) are a class of large lipoprotein synthesized in the liver and are used by the adrenal gland as a source of cholesterol. Researchers at Georgia Health Sciences and the Charlie Norwood Veteran’s Affairs Medical Center used primary cultures of human and bovine adrenal cells and the adrenocortical cell line H295R as models to determine the effects of VLDL on adrenal steroidogenesis. Adrenal cells exposed to physiological concentrations of VLDL (Kalen Biomedical and others) in culture expressed increased levels of StAR protein and aldosterone synthase. The presence of calcium channel blocker, Nifedipine inhibited the increase in CYP11B2 mRNA expression, suggesting that calcium is the main signal transduction pathway used by VLDL in adrenal cells. The primary cultures that were exposed to physiological concentrations of VLDL for 48 hrs increased aldosterone production approximately two-fold.
“Adrenal Cell Aldosterone Production Is Stimulated by Very-Low-Density Lipoprotein (VLDL).”
Endocrinology. 2012 Feb;153(2):721-31. doi: 10.1210/en.2011-1752. Epub 2011 Dec 20.
Xing Y, Rainey WE, Apolzan JW, Francone OL, Harris RB, Bollag WB.
Department of Physiology, Georgia Health Sciences University, 1120 15th Street, Augusta, Georgia 30912, USA.