Despite the prevalence of dyspepsia, nonhuman models for study of gastric hyperalgesia are limited. We thus characterized responses to gastric distension (GD) in the absence of and after two different gastric insults. A balloon was surgically placed into the stomach, and electromyographic responses to GD were recorded from the acromiotrapezius muscle at various times after balloon placement. Rats received either 20% acetic acid (HAc) or saline injections into the stomach wall or 0.1% iodoacetamide (IA) in drinking water. Responses to GD were monotonic with increasing distending pressure (10–80 mmHg) and were reproducible from days 3–14 after balloon implantation. Both HAc injection and IA ingestion led to increased responses to GD (i.e., gastric hyperalgesia), which, in the case of HAc, persisted for 60 days after HAc treatment. HAc injection produced ulcers in all treated animals; IA ingestion produced no lesions. Myeloperoxidase activity significantly increased after HAc but not saline injection or IA ingestion. In the awake, unrestrained rat, visceromotor responses to GD are quantifiable, reliable, and reproducible. Significantly enhanced responses to GD were apparent in two models of gastric insult, both of which may be useful for the study of the mechanisms of gastric hyperalgesia.