NPS 2390 is a group I mGlu antagonist; displays noncompetitive antagonist activity at both mGlu1 and mGlu5 receptors. Thought to act on a site separate from the glutamate binding pocket. GdCl(3), an activator of CaR, and NPS-2390, a specific inhibitor, were administered. The PC and PC (post-conditioning) with NPS-2390 groups improved the recovery of cardiac function during reperfusion compared to the IR and PC groups with GdCl(3), respectively[1]. The intracellular calcium concentration ([Ca(2+)](i)) was increased by an increment of [Ca(2+)](o). This [Ca(2+)](i) increment was inhibited by the pretreatment with NPS 2390, an antagonist of CaSR (calcium sensing receptor)[2]. Calcium oxalate increased OS, crystal adhesion, PS ectropion, and the expression of CaSR and ERK, OPN, and KIM-1 in vivo. In addition, lower levels of urine citrate as well as increased serum creatinine and urea levels were observed after treatment with calcium oxalate (p < .05). Compared with calcium oxalate treatment alone, the above deleterious changes were further significantly confirmed by GdCl3 but were reversed by NPS-2390. However, urine calcium excretion was decreased after ethylene glycol treatment but was significantly reduced by NPS 2390 and increased by GdCl3 (p < .05)[3].
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