RESUMO
In order to compare the effects of several experimental renal calcium oxalate stones formation models in rats and to find a simple and convenient model with significant effect of calcium oxalate crystals deposition in the kidney, several rat models of renal calcium oxalate stones formation were induced by some crystal-inducing drugs (CID) including ethylene glycol (EG), ammonium chloride (AC), vitamin D(3)[1alpha(OH)VitD(3), alfacalcidol], calcium gluconate, ammonium oxalate, gentamicin sulfate, L-hydroxyproline. The rats were fed with drugs given singly or unitedly. At the end of experiment, 24-h urines were collected and the serum creatinine (Cr), blood urea nitrogen (BUN), the extents of calcium oxalate crystal deposition in the renal tissue, urinary calcium and oxalate excretion were measured. The serum Cr levels in the stone-forming groups were significantly higher than those in the control group except for the group EG+L-hydroxyproline, group calcium gluconate and group oxalate. Blood BUN concentration was significantly higher in rats fed with CID than that in control group except for group EG+L-hydroxyproline and group ammonium oxalate plus calcium gluconate. In the group of rats administered with EG plus Vitamin D(3), the deposition of calcium oxalate crystal in the renal tissue and urinary calcium excretion were significantly greater than other model groups. The effect of the model induced by EG plus AC was similar to that in the group induced by EG plus Vitamin D(3). EG plus Vitamin D(3) or EG plus AC could stably and significantly induced the rat model of renal calcium oxalate stones formation.
Assuntos
Oxalato de Cálcio/urina , Cálculos Renais/metabolismo , Rim/metabolismo , Cloreto de Amônio/efeitos adversos , Cloreto de Amônio/metabolismo , Cloreto de Amônio/urina , Animais , Nitrogênio da Ureia Sanguínea , Cálcio/sangue , Cálcio/metabolismo , Cálcio/urina , Gluconato de Cálcio/efeitos adversos , Gluconato de Cálcio/metabolismo , Gluconato de Cálcio/urina , Oxalato de Cálcio/metabolismo , Creatinina/sangue , Cristalização , Modelos Animais de Doenças , Etilenoglicol/efeitos adversos , Etilenoglicol/metabolismo , Etilenoglicol/urina , Gentamicinas/efeitos adversos , Gentamicinas/metabolismo , Gentamicinas/urina , Hidroxicolecalciferóis/efeitos adversos , Hidroxicolecalciferóis/metabolismo , Hidroxicolecalciferóis/urina , Hidroxiprolina/efeitos adversos , Hidroxiprolina/metabolismo , Hidroxiprolina/urina , Rim/patologia , Cálculos Renais/induzido quimicamente , Cálculos Renais/prevenção & controle , Magnésio/metabolismo , Magnésio/urina , Masculino , Microscopia de Polarização , Oxalatos/efeitos adversos , Oxalatos/metabolismo , Oxalatos/urina , Fósforo/sangue , Distribuição Aleatória , Ratos , Ratos WistarRESUMO
The calcium-sensing receptor (CaSR) has been detected in human antral gastrin-secreting cells, where, upon calcium and/or amino acid allosteric activation, it stimulates gastrin secretion. Patients with absorptive hypercalciuria (AH) display an enhanced gastric acid output; therefore, we evaluated the secretion of gastrin in subjects with AH (30 subjects vs. 30 healthy female controls, all postmenopausal) after oral calcium administration (1 g calcium gluconate) and, on a separate occasion, after peptone loading test (protein hydrolyzed, 10 g). Gastrin and monomeric calcitonin responses were higher in AH after both oral calcium administration (P < 0.01) and peptone loading (P < 0.01). Because the activation of CaSR by oral calcium and peptones directly induces gastrin release, the higher gastrin responses to these stimuli suggest an increased sensitivity of gastrin-secreting cells CaSR in patients with AH. A similar alteration in thyroid C cells might explain the enhanced calcitonin responses to both calcium and peptones. If the same alterations should in addition be present in the distal tubule (where CaSR is expressed as well), then a possible explanation for amino acid-induced hypercalciuria in AH would have been identified.
