Many gastrointestinal complications in diabetes are connected to neurohumoral dysfunction resulting in abnormalities of intestinal motility, secretion and absorption. Minerals have been reported as essential cofactors for basic cellular reactions but there is dearth of information on effect of Magnesium on gastrointestinal transit time (GITT) and the mechanism of action. Sixty male albino Wistar rats (180 - 200g) were grouped into twelve of five animals each. Group 1 (control) received 0.2ml saline. Groups 2-6 were normal rats treated with magnesium sulphate (as magnesium) (500mg/kg), adrenaline (0.5mg/kg), magnesium (500mg/kg) and adrenaline (0.5mg/kg), prazosin (1mg/kg) and both magnesium (500mg/kg) and prazosin (1mg/kg) respectively. Groups 7 - 12 were diabetic rats treated as in groups 1- 6. Diabetes was induced intraperitoneally with alloxan (120mg/kg bwt). There was significant (p<0.05) reduction in GITT index in normal rats treated with magnesium, prazosin and combination of magnesium and prazosin compared with control. Treatment with adrenaline alone produced significant increase in GITT. However treatment with both magnesium and adrenaline produced significant reduction compared with control. This reduction in GITT was similar to that obtained in magnesium only and prazosin only treated groups. Diabetic groups showed significant reduction in GITT in all treated groups except the adrenaline only treated group which produced significant increase in GITT. The significant reduction in GITT produced by magnesium in both normal and diabetic animals was comparable to that produced by prazosin (an á-adrenoceptor antagonist) indicating that magnesium may be inhibiting gastrointestinal smooth muscle contraction through á-adrenoceptor antagonist pathway.