Efeitos do fator estimulador de colônias de Granulócitos (g-csf) sobre a hipertensão renovascular em Camunongos

• Autor(a) principal: Nogueira, Breno Valentim
• Data de Publicação: 2008
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Repositório Institucional da Universidade Federal do Espírito Santo (riUfes)
• Texto Completo: http://repositorio.ufes.br/handle/10/5156
• topic: Renovascular hypertension; kidney infarct; G-CSF; Hipertensão renovascular; Ang II; infarto renal; Fisiologia; 612

Background: The hematopoietic cytokine granulocyte colony-stimulating factor (GCSF) is a critical regulator of myeloid progenitor cell proliferation, differentiation and survival. And also, causes a marked increase in the mobilization of hematopoietic stem cells into the peripheral blood circulation. Recently, several studies regarding the effect of G-CSF attenuate renal injury during episode of acute ischemia-reperfusion. Aims: To evaluate the effects of G-CSF treatment into renal and cardiovascular system of mice with two-kidney, one-clip (2K1C) hypertension. Methods: Male C57 mice received a clip (0.12 mm) on the renal artery to induce renovascular hypertension (C57-2K1C, n = 32). All groups received G-CSF (100 µg/kg/day, SC) for 14 days since the operation. After treatment, the hemodynamic parameters were measured in conscious animals. At the end of the experiment the sample blood was collected and animals were euthanized in CO2 chamber. Also, the kidneys, hearts and others organs were excised, drained, and weighed. All values are expressed as mean±SEM. Two-way ANOVA was used to detect differences within each experimental group followed by post hoc Fisher test. Student’s t-test for independent samples was used when appropriate. Statistical significance was defined as p<0.05. Results: The animals 2K1C G-CSF showed that mean arterial pressure was lower than observed in 2K1C vehicle (129±2** mmHg vs. 150±5 mmHg, n=8). The clipped kidney/ contralateral kidney ratio showed a less atrophy of the ischemic kidney in treated group (0.50±0.02 vs. 0.66±0.01*). In addition, the histopathological analyses of kidney reveal a minor kidney infarct area with G-CSF use. The levels of plasma angiotensin I, II and 1-7 showed elevation in 2K1C vehicle when compared to sham group. However, we observed down levels of angiontensin I and 1-7 in 2K1C treated group. The infarct areas include 54% of all clipped kidney area, this areas reduced to 14% with G-CSF treatment. Conclusion: In conclusion, our data indicate that G-CSF administration prevents the kidney infarct and attenuate the high arterial blood pressure in 2K1C hypertensive mice, reinforcing the protect role of G-CSF on the kidney ischemia.