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[Regulation of the calcium-sensing receptor. Influence of secondary hyperparathyroidism]. / Regulación del receptor sensor de calcio. Influencia del hiperparatiroidismo secundario.
Fernández Martín, J L; González Suárez, I; Cannata Andía, J B.
Afiliação
  • Fernández Martín JL; Servicio de Metabolismo Oseo y Mineral, Instituto Reina Sofía de Investigación, Hospital Universitario Central de Asturias, Universidad de Oviedo, Oviedo.
Nefrologia ; 23 Suppl 2: 7-11, 2003.
Article em Es | MEDLINE | ID: mdl-12778846
The parathyroid glands have a great sensitivity to small changes in the extracellular ionic calcium. The calcium-sensing receptor (CaR) is a G protein-coupled receptor that responds to extracellular ionic calcium changes activating several intracellular signalling systems (phospholipases C, A2 and D) finally inhibiting the PTH secretion. In addition to calcium, there are some other agonists and modulators such as the Mg2+, spermine, amyloid beta-peptides, a variety of aminoacids, especially aromatic aminoacids and ionic strength. In the uraemia, the sensitivity of the parathyroid glands to calcium is altered and higher values of calcium are necessary to suppress the PTH. In the secondary hyperparathyroidism the CaR expression is reduced. It has been found a negative correlation between cellular proliferation and the expression of the CaR in hyperplasic glands. Despite it is a calcium receptor, the expression of the CaR does not seem to be regulated by calcium and there is some controversy about the role of calcitriol regulating its expression. On the other hand, the phosphorous induces hyperplasia of the parathyroid gland increasing the cellular proliferation and a decrease of the CaR expression.
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Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Etiology_studies Limite: Animals / Humans Idioma: Es Ano de publicação: 2003 Tipo de documento: Article
Buscar no Google
Coleções: 01-internacional Base de dados: MEDLINE Tipo de estudo: Etiology_studies Limite: Animals / Humans Idioma: Es Ano de publicação: 2003 Tipo de documento: Article