Related Experiment Video
Updated: Sep 10, 2025

A Large Animal Model for Acute Kidney Injury by Temporary Bilateral Renal Artery Occlusion
Published on: February 2, 2021
Renal Effects and Nitric Oxide Response Induced by Bothrops atrox Snake Venom in an Isolated Perfused Kidney Model
Terentia Batista Sa Norões1, Antonio Rafael Coelho Jorge2, Helena Serra Azul Monteiro2
1Department of Medicine, Centro Universitário Doutor Leão Sampaio (UNILEÃO), Maria Letícia Leite Pereira Ave., Lagoa Seca-Cidade Universitária, Juazeiro do Norte 63040-405, CE, Brazil.
Abstract:
The snakes from the genus Bothrops are responsible for most of the ophidic accidents in Brazil, and Bothrops atrox represents one of these species. Envenomation by these snakes results in systemic effects and is often associated with early mortality following snakebite incidents. The present study investigates the pharmacological properties of Bothrops atrox venom (VBA), focusing specifically on its impact on renal blood flow. Following the renal perfusion procedure, kidney tissues were processed for histopathological examination. Statistical analysis of all evaluated parameters was conducted using ANOVA and Student's t-test, with significance set at p < 0.005. Administration of VBA resulted in a marked reduction in both perfusion pressure and renal vascular resistance. In contrast, there was a significant elevation in urinary output and glomerular filtration rate. Histological changes observed in the perfused kidneys were mild. The involvement of nitric oxide in the pressor effects of Bothrops atrox venom was not investigated in renal perfusion systems or in in vivo models. Treatment with VBA led to elevated nitrite levels in the bloodstream of the experimental animals. This effect was completely inhibited following pharmacological blockade with L-NAME. Based on these findings, we conclude that VBA alters renal function and promotes increased nitric oxide production.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Acute Kidney Injury II: Pathophysiology

