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• W2032369929 abstract "Mechanism of concentrating defect in hypercalcemia. Role of polydipsia and prostaglandins. This study investigates the mechanism of the renal concentrating defect in a model of chronic hypercalcemia in the rat (serum calcium 12.4 ± 0.2mg %). Maximal urinary osmolality was 1669 ± 76 mOsm/kg H 2 O in hypercalcemic rats as compared to 2609 ± 61 mOsm/kg H 2 O in pair-fed controls, P 2 excretion was increased markedly in both ad lib water and pair-watered hypercalcemic rats as compared to controls, the role of prostaglandin E 2 in the renal concentrating defect was investigated by determining the maximal urinary concentration following prostaglandin inhibition achieved by administration of indomethacin. Prostaglandin inhibition failed to improve the renal concentrating defect in hypercalcemic rats. Our study therefore demonstrates that chronic hypercalcemia causes renal concentrating defect of nephrogenic origin that is partially dependent on the associated polydipsia and polyuria. The polyuria-polydipsia independent component of the defect is associated with decreased inner medullary tissue solute content. Despite very high prostaglandin E 2 excretion rates, the renal concentrating defect appears to be prostaglandin independent. Mecanisme du defaut de concentration dans l'hypercalcemie. Role de la polydipsie et des prostaglandines. Ce travail etudie le mecanisme du defaut de concentration renale dans un modele d'hypercalcemie chronique chez le rat (calcemies 12,4 ± 0,2mg %). L'osmolalite urinaire maximale etait de 1669 ± 76 mOsm/kg H 2 O chez les rats hypercalcemiques par rapport a 2609 ± 61 mOsm/kg H 2 O chez des controles nourris de facon appariee, P 2 etait augmentee de facon marquee chez les rats hypercalcemiques recevant de l'eau ad libitum ou de facon appariee par rapport aux controles, le role de la prostaglandine E 2 dans le defaut de concentration renale a ete etudie en determinant la concentration urinaire maximale apres inhibition des prostaglandines par administration d'indomethacine. L'inhibition des prostaglandines n'a pas permis d'ameliorer le defaut de concentration renale chez les rats hypercalcemiques. Notre etude demontre donc que l'hypercalcemie chronique entraine un defaut de concentration renale d'origine nephrogene. Ce defaut de concentration renale est partiellement dependant de la polydipsie et de la polyurie associees. La composante independante de la polyurie et de la polydipsie de ce defaut est associee avec une diminution du contenu en solutes tissulaires medullaires internes. Malgre des debits d'excretion de prostaglandines E 2 tres eleves, le defaut de concentration renale semble etre independant des prostaglandines." @default.
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• W2032369929 title "Mechanism of concentrating defect in hypercalcemia. Role of polydipsia and prostaglandins" @default.
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