Premenopausal women have a lower cardiovascular risk than men or postmenopausal women. However, this "female advantage" is lost in diabetes, a condition characterized by cardiac and vascular contractile dysfunction. This study was designed to compare the influence of diabetes on vascular and myocardial contractile function between genders. Adult male and female rats were made diabetic with streptozotocin (55 mg/kg) and maintained for 8 weeks. Tension development was examined in thoracic aortic rings and left ventricular papillary muscles. KCl-induced vasoconstriction, acetylcholine (ACh)-induced endothelium dependent or sodium nitroprusside (SNP)-induced endothelium-independent vasorelaxation, duration and maximal velocity of myocardial contraction and relaxation duration (TPT/RT90 and +/- VT) were similar between males and females. Diabetes augmented KCl-induced vasoconstriction at low doses, reduced SNP-induced vasorelaxation and had little effect on ACh-induced vasorelaxation in aortic rings from both genders. Diabetes prolonged TPT and RT90 in both genders, and reduced +/- VT in males but not females. Acute increase in extracellular Ca2+ (2.7 mM to 5.4 mM) shortened TPT in diabetic myocardium from both genders, whereas it had no effect on other myocardial mechanical indices in normal or diabetic groups of either gender. In addition, acute exposure to the Na+/K(+)-ATPase inhibitor ouabain shortened TPT/RT90 and enhanced +/- VT in myocardium from normal female, whereas it had no effect on male or diabetic myocardium. In conclusion, these data suggest that in the vasculature, there is no difference in diabetes-induced contractile dysfunction between genders, however several gender-specific differences are evident in the myocardium.