Aumento dos níveis pressóricos e alteração da resposta de contração vascular em artéria renal de ratos wistar após tratamento crônico com prednisona

Abstract

The Prednisone (PRD) is a synthetic corticoid which provokes several effects in the systemic blood pressure and in the vascular contraction. It is possible to enlarge the findings about which factors this drug modulate the function and the blood pressure (PA) in the renal arteries (AR). This study’s goal is to evaluate the effect of the chronic treatment of the PRD on the blood pressure levels and also on the function of the vascular contraction on the AR in healthy rats. An experiment was performed with male rats of the Wistar lineage, weighing between 190 and 210 grams, being 15-16 weeks old, divided in a control group treated with vehicle (VEI; n= 7 rats), and treated with prednisone (PRD; n= 7 rats) with the dose of 5,0mg/Kg during 17 days by intragastric route (gavage). The systolic PA was held, after the animals’ deaths, the segments of the thoracic aorta were evaluated with Phenylephrine (FE), and then with serotonine (5-HT). The concentration-response curves for FE were performed respectively in the presence or the absence of the L-NAME [a nonspecific inhibitor of the nitric oxide synthase (NOS)], and INDO (a nonspecific inhibitor of the COX), taking in account two pharmacological parameters: the maximum effect generated by the agonist (or Emax) and –log EC50 (or pD2). The results were expressed with the average ± average standard error (EPM). The statistical analyses was determined by the ANOVA One Way test and the Tukey post-test, for analysis between 3 groups or for more different samples, or T student test for comparison between two groups, through the Graph Pad Prism 5.0 program (GraphPad Software Incorporated, CA) and the values of P<0,05 were considered statistically significant. It was observed that the chronic treatment with the PRD modifies the response of the AR vascular contraction when induced by the FE, as well as their blood pressure levels. The increase of the sensibility observed in the AR is dose-dependent for the FE. The AR vascular contraction response in the PRD group only occurs with the agonist α-adrenergic and the inhibition of the NO route, by the L-NAME, provokes an increase of the sensibility of the contraction in the VEI group, and removes the difference in the sensibility to Fe observed in the PDR group versus the control group. As for the inhibition of the COX route, by the INDO, the maximum response is reduced in both groups, and the difference in sensibility to FE observed in the group PDR versus the control group is removed. It is concluded that the chronic use of the PRD changes the PAS and the contraction function of the AR. Also, it is evident that the PRD just induces a sensibility to the AR constant contraction, but did not change the maximum contraction of the vase, due to the PRD harms the NO synthesis and the production of some products of the COX.