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Am J Physiol Renal Physiol (April 8, 2009). doi:10.1152/ajprenal.90557.2008
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Submitted on September 17, 2008
Revised on March 30, 2009
Accepted on April 5, 2009

N-Methyl-D-Aspartate Receptors Are Expressed In Rat Parathyroid Gland And Regulate PTH Secretion

Eva Parisi1, Yolanda Almaden, Merce Ibarz, Sara Panizo, Anna Cardus, Mariano Rodriguez2, Elvira Fernandez, and Jose Manuel Valdivielso3*

1 University of California San Diego and VA San Diego Healthcare System
2 Hospital Universitario Reina Sofa
3 Hospital Universitario Arnau de Vilanova. IRBLLEIDA

* To whom correspondence should be addressed. E-mail: valdivielso{at}medicina.udl.es.

N-methyl-D-aspartate receptors (NMDAR) are tetrameric amino acid receptors which act as membrane calcium channels. The presence of the receptor has been detected in the principal organs responsible for calcium homeostasis (kidney and bone), pointing to a possible role in mineral metabolism. In the present work the presence of the receptor was determined in normal parathyroid glands (PTG) by real-time PCR, immunoprecipitation and immunohistrochemistry. Healthy animals showed a decrease in blood PTH levels 15 minutes after the treatment with NMDA. This effect was also observed in animals with high levels of PTH induced EDTA injection, but not in uremic animals with secondary hyperparathyroidism (2HPT). Normal rat PTG incubated in media with low calcium concentration (0.8 mM CaCl2) showed a decrease in PTH release when NMDA was added to the media. This effect of NMDA was abolished when glands were coincubated with MK-801 (a pharmacological blocker of the NMDA channel) or PD 98059 (an inhibitor of the ERK-MAPK pathway). Glands obtained from animals with 2HPT showed no effect of NMDA in the in vitro release of PTH, together with a decrease in the expression of NMDAR1. In conclusion, NMDA receptor is present in PTG and is involved in the regulation of the PTH release. The mechanism by which NMDAR exerts its function is through the activation of the MAPK cascade. In uremic 2HPT animals the receptor expression is downregulated and the treatment with NMDA does not affect PTH secretion.






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