Rats were rendered diabetic by a single administration of streptozotocin (STZ). They were maintained in the diabetic state for six weeks before being killed, and diabetic state was confirmed by routine urine and blood glucose estimations. The contractile sensitivity of jejunum, colon, stomach fundus and uterus to carbachol was reduced in control animals by increasing buffer magnesium concentration from 1.9 mmol/litre to 23.8 mmol/litre. This magnesium effect was reversed in the colon, stomach fundus and uterus of streptozotocin-diabetic animals, with contractile sensitivity being enhanced in the presence of increased magnesium concentration. In the jejunum, however, the magnesium effect was not reversed by STZ-induced diabetes. In diabetic animals, magnesium generally had the opposite effect on gastrointestinal and uterine tissues when compared with control animals. This suggests that, in the diabetic condition, any altered gastrointestinal function may be due to an underlying difference in the sensitivity to changes in magnesium.