Is atorvastatin-induced increase in progenitor cell levels rather caused by enhanced receptor activator of NF-kappaB ligand ( RANKL ) cell proliferation than by bone marrow mobilization?
Atorvastatin treatment increases RANKL levels with no measurable effect on bone metabolism and mobilization of progenitor cells from BM to PB. RANKL is essential for the statin-mediated increase of progenitor cell levels but predominantly due to a RANKL-induced stimulation of cell proliferation.
In contrast to studies performed in the vasculature of the human forearm or the coronary circulation, our results suggest that hypercholesterolaemia is not associated with an impaired L-arginine-induced renal vascular relaxation.