Background: Consumption of high-glycemic index foods contributes to the development of hypertension in some patients. Likewise, in spontaneously hypertensive rats (SHR), high sucrose promotes a secondary rise in systolic blood pressure (SBP). Chromium (III) (Cr³⁺) prevents sucrose-induced hypertension, but leaves the basal hypertension that characterizes SHR intact. Methods: Since hypertension entails increased peripheral resistance, we compared effects of Cr³⁺ on resistance arteries from SHR fed low-glycemic (starch) versus high-glycemic (sucrose) index diets. Subgroups of SHR also received Cr³⁺. Structure, stiffness, and vasodilation of mesenteric resistance arteries were studied using pressurized myography. Results: Sucrose increased SBP in SHR and, exclusively in sucrose-fed SHR, Cr³⁺ reduced SBP and augmented acetylcholine or nitroprusside-dependent vasodilation. Neither sucrose nor Cr³⁺ affected artery structure or stiffness. Since Cr³⁺ enhanced vasodilation, we assessed endothelial NO synthase (eNOS), guanylate cyclase, cGMP-dependent protein kinase (PKG-1α and 1β), and PKG activity by immunoblotting. Sucrose reduced eNOS, PKG-1β, and PKG activity. Cr³⁺ prevented the effects of sucrose on NO signaling. Conclusion: In hypertension exacerbated by high-glycemic index diet, Cr³⁺ reduces SBP. The BP-lowering effect of Cr³⁺, selectively on sucrose-induced but not basal hypertension in SHR, involves at least in part, improving vasodilatory function vis-à-vis restoration of NO signaling in resistance arteries.