Effect of dietary chromium on resistance artery function and nitric oxide signaling in the sucrose-fed spontaneously hypertensive rat.
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) (Cr(3+)) prevents sucrose-induced hypertension, but leaves the basal hypertension that characterizes SHR intact.


METHODS
Since hypertension entails increased peripheral resistance, we compared effects of Cr(3+) on resistance arteries from SHR fed low-glycemic (starch) versus high-glycemic (sucrose) index diets. Subgroups of SHR also received Cr(3+). 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, Cr(3+) reduced SBP and augmented acetylcholine or nitroprusside-dependent vasodilation. Neither sucrose nor Cr(3+) affected artery structure or stiffness. Since Cr(3+) enhanced vasodilation, we assessed endothelial NO synthase (eNOS), guanylate cyclase, cGMP-dependent protein kinase (PKG-1alpha and 1beta), and PKG activity by immunoblotting. Sucrose reduced eNOS, PKG-1beta, and PKG activity. Cr(3+) prevented the effects of sucrose on NO signaling.


CONCLUSIONS
In hypertension exacerbated by high-glycemic index diet, Cr(3+) reduces SBP. The BP-lowering effect of Cr(3+), 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.
Kopilas
Melanie A
MA
Canadian Centre for Agri-Food Research in Health and Medicine, St. Boniface Hospital Research Centre, Winnipeg, Manitoba, Canada.
Dang
Lam N T
LN
Anderson
Hope D I
HD
D000821:Animal Feed; D000818:Animals; D002857:Chromium / Q000494:pharmacology*; D006152:Cyclic GMP / Q000378:metabolism; D019422:Dietary Sucrose / Q000494:pharmacology; D006973:Hypertension / Q000188:drug therapy* / Q000378:metabolism; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR; D015398:Signal Transduction / Q000502:physiology*; D013213:Starch / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects*
D019422:Dietary Sucrose; D002857:Chromium; D009569:Nitric Oxide; D013213:Starch; D052250:Nitric Oxide Synthase Type III; D006152:Cyclic GMP