RESUMEN
Kidney failure is the common end of hypertension and renal diseases. Several authors have suggested that vasodilatory prostaglandins participate in the hemodynamic mechanism responsible for the development of kidney failure. However, the mechanism by which prostaglandins are increased in renal disease is not clear. Recently, 2 isoforms of the enzyme responsible for prostaglandin synthesis, cyclooxygenase, have been described as cyclooxygenase-1 (COX-1), a constitutive isoform, and cyclooxygenase-2 (COX-2), an inducible isoform. In the present study, we investigated whether COX-2-dependent prostaglandins participate in the evolution of renal functional changes after renal ablation. We inhibited prostaglandin synthesis by COX-1 and COX-2 with indomethacin (3 mg/kg) and prostaglandin synthesis by COX-2 with NS-398 (3 mg/kg) and tested the effect of these inhibitors on the renal functional changes elicited by renal ablation. Renal ablation produced an increase in urinary volume, protein, and prostaglandin E(2), whereas urinary sodium and potassium were not affected and urinary osmolarity decreased; treatment with indomethacin or NS-398 partially prevented the renal functional changes elicited by renal ablation. Immunoblots for COX showed an increase in the expression of COX-2 protein 2 days after renal ablation. Furthermore, COX-2 mRNA expression was increased 1 day after renal ablation. These data suggest that COX-2-dependent prostaglandins participate in the renal mechanisms associated with the development of renal functional changes after renal ablation.
Asunto(s)
Inhibidores de la Ciclooxigenasa/farmacología , Dinoprostona/fisiología , Indometacina/farmacología , Isoenzimas/fisiología , Nitrobencenos/farmacología , Prostaglandina-Endoperóxido Sintasas/fisiología , Insuficiencia Renal/metabolismo , Sulfonamidas/farmacología , Animales , Ciclooxigenasa 1 , Ciclooxigenasa 2 , Inhibidores de la Ciclooxigenasa 2 , Inhibidores de la Ciclooxigenasa/uso terapéutico , Indometacina/uso terapéutico , Pruebas de Función Renal , Masculino , Proteínas de la Membrana , Nitrobencenos/uso terapéutico , Ratas , Ratas Wistar , Insuficiencia Renal/fisiopatología , Insuficiencia Renal/prevención & control , Sulfonamidas/uso terapéuticoRESUMEN
Preliminary results of active immunotherapy ,both in vitro and in vivo, about ascitical Ehrlich carcinoma transplanted in albinic swiss mice are presented. In the in vitro experiment, tumor cells were marked with the immunoglobulin, anti-tumor-associated antigens (TAA) and were coupled to a dinitrophenyl radical (Ig DNP anti-TAA). These cells were meaningfully hindered from migration in presence of swiss albinic mice's splenic cells. These mice were sensibilized to the tumor cells marked with Ig-DNP. The injection of a Ig-DNP anti-TAA 0,3 ml, every third days, intraperitoneal way, in a span of 21 days, in albinical swiss mice with a transplant of 3 X 10(5) Ehrlich carcinoma cells (group A) 24 hours before, constituted the in vivo test. The growth ought to be compared to an Ig-DNP tolerant group (group B), which received equal quantities of tumor cells and followed the same plan of treatment, as well as to another control group transplanted under the same conditions, but with no treatment (group C). Eight days from the experiment, there was a clear difference between group A and groups B and C. The last two groups died from 13th to the 26th day after the transplant. On the contrary, the whore group A continued alive and with no sign of ascitical tumor. Nevertheless, an animal of group A died after the 28th day, due to a solid tumor in the abdominal wall.