<unk>  increases blood<unk> cium levels () by: * Promoting absorption of dietary<unk> cium from the gastrointestinal tract. * Increasing renal tubular reabsorption of<unk> cium, thus reducing the loss of<unk> cium in the urine. * Stimulating release of<unk> cium from bone. For this it acts on the specific type of bone cells referred to as osteoblasts, causing them to release RANKL, which in turn activates osteoclasts.<unk>  acts in concert with parathyroid hormone (PTH) in all three of these roles. For instance, PTH also indirectly stimulates osteoclasts. However, the main effect of PTH is to increase the rate at which the kidneys excrete inorganic phosphate (Pi), the counterion of . The resulting decrease in serum phosphate causes hydroxyapatite (Ca5(PO4)3OH) to dissolve out of bone, thus increasing serum<unk> cium. PTH also stimulates the production of<unk>  (see below). Many of the effects of<unk>  are mediated by its interaction with the<unk>  receptor, also<unk> led the vitamin D receptor or VDR. For instance, the unbound inactive form of the<unk>  receptor in intestinal epithelial cells resides in the cytoplasm. When<unk>  binds to the receptor, the ligand-receptor complex translocates to the cell nucleus, where it acts as a transcription factor promoting the expression of a gene encoding a<unk> cium binding protein. The levels of the<unk> cium binding protein increase enabling the cells to actively transport more<unk> cium () from the intestine across the intestinal mucosa into the blood. Alternative, non-genomic pathways may be mediated through either PDIA3 or VDR. The maintenance of electroneutrality requires that the transport of ions catalyzed by the intestinal epithelial cells be accompanied by counterions, primarily inorganic phosphate. Thus<unk>  also stimulates the intestinal absorption of phosphate. The observation that<unk>  stimulates the release of<unk> cium from bone seems contradictory, given that sufficient levels of serum<unk>  generally prevent overall loss of<unk> cium from bone. It is believed that the increased levels of serum<unk> cium resulting from<unk> -stimulated intestinal uptake causes bone to take up more<unk> cium than it loses by hormonal stimulation of osteoclasts. Only when there are conditions, such as dietary<unk> cium deficiency or defects in intestinal transport, which result in a reduction of serum<unk> cium does an overall loss of<unk> cium from bone occur.<unk>  also inhibits the release of<unk> citonin, a hormone which reduces blood<unk> cium primarily by inhibiting<unk> cium release from bone.
Calcitriol
Parathyroid hormone
Estriol
Estriol 
Parathyroid hormone-related protein
Cholecalciferol
Ergocalciferol
Calcipotriol