Study On The Regulation Of Cerebral Arterial BK Channels By Angiotensin Ⅱ Signaling In Adult Offspring Exposed To Prenatal High-Sucrose Diets

Background:The ‘fetal programming’ hypothesis proposed by Barker postulated that factors operative during organogenesis caused long-lasting effects persisting during adult life. High sucrose intake causes insulin resistance, adverse cardiovascular outcomes and potentially also blood pressure(BP)-independent target organ damage. Excess sucrose intake in pregnancy is known to affect vascular responses in the offspring. The present study was designed to assess whether high sucrose intake in pregnancy affects vascular functions in the offspring.Methods: Sprague–Dawley rats were fed a standard food and tap water with normal or high(20%) sucrose content during pregnancy. After weaning, all offspring were maintained on the normal diet and tap water. Vascular function was assessed in male offspring at 20-24 weeks postnatal.Results: Angiotensin II(Ang II)-induced vasoconstrictions were significantly higher in the high-sucrose offspring. BK Currents are reduced in the HS group. High-sucrose composition in sub cultured rat, AT1 a and AT2 receptor m RNA expression of brain artery were significantly higher than those of the control group(P < 0.05),and BKβ1 receptor m RNA expression of brain artery was significantly lower than those of the control group(P < 0.05),AT1 b and BKα receptor m RNA expression had no statistical difference(P > 0.05). The m RNA AT1:AT2 expression ratio increased significantly compared with the expression level in the edible high sucrose generation.Conclusions: Our study suggested that prenatal exposed to HS altered micro-vascular activity in MCA probably via changes in BK channels mediated AngⅡ signaling pathways, which may lead to increased risks of stroke in the offspring.