PMID: 16521071Mar 8, 2006Paper

Calcimimetics

Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia
Piergiorgio MessaB Brezzi

Abstract

Current therapy for secondary hyperparathyroidism in uremia has relatively poor success in achieving the target levels of parathyroid hormone (PTH), calcium and phosphate established by the NKF-K/DOQI guidelines. The discovery and characterization of a new membrane receptor able to sense minimal Ca changes (CaSR) started intensive research in the attempt to characterize better its functions and its finding compounds, which could modulate its activity. CaSR is expressed not only in the cells that secrete calcium-regulating hormones (parathyroid cells and thyroid C-cells) and in cells involved in calcium transport mechanisms (ie intestinal cells, bone-forming osteoblasts, and cells of different nephron segments), but also in other tissues with, as yet, a not completely defined role. CaSR stimulation by the agonists is followed by the activation of a great number of G-proteins mediated intracellular signalling pathways (PLC, PLA, PLD, PKC, PKA, etc). At the level of parathyroid cells, the main effect is the increase in IP3, followed by a mobilization of intracellular Ca stores, which inhibit PTH secretion in a few seconds or minutes. Long-term CaSR stimulation is also able to induce a reduction in both PTH synthesis and parathyroi...Continue Reading

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