Figure 3. SIN-1-induced vasodilatation.

A, in the presence of Ringer solution. The vasodilatory response to SIN-1 was unaffected by diabetes and maturation. Blood pressure values in age-matched controls and STZ-induced diabetics were not significantly different at any age. B, in the presence of l-NNA + indomethacin (1 mm + 10⁻⁵m). The response to SIN-1 declined with maturation in age-matched controls (⁺P = 0.0134, analysis for linear trend), but not in STZ-induced diabetics. Blood pressure values in age-matched controls and STZ-induced diabetics were not significantly different at any age. C, in the presence of TEA + l-NNA + indomethacin (10 mm + 1 mm + 10⁻⁵m). A significant difference in the magnitude of the SIN-1 responses between age-matched controls and STZ-induced diabetics emerged after application of TEA subsequent to l-NNA + indomethacin. Under these conditions, the SIN-1 response declined with maturation (⁺⁺P = 0.0011, analysis for linear trend) in age-matched controls, but was equally depressed in all STZ-induced diabetic groups. The difference between control and diabetic responses to SIN-1 in the presence of TEA + l-NNA + indomethacin (**P = 0.001, two-way ANOVA) demonstrates impaired reactivity of the NO-cGMP pathway to exogeneous NO in STZ-induced diabetes. This impairment occurred immediately after induction of diabetes in the 1–2 week group, was transient, and was no longer apparent in the 18–20 week group. At this point in the experimental protocol, significant differences between age-matched control and STZ-induced diabetic blood pressure values were found, but only between the 8–10 week groups (controls: 98.9 ± 6.0 mmHg; diabetics: 118.5 ± 6.4 mmHg). The data in all three panels are given as means and 95 % confidence intervals.