Intake of high sucrose during pregnancy altered large-conductance Ca2+-activated K+ channels and vessel tone in offspring's mesenteric arteries.

Antenatal malnutrition could be linked to hypertension and vascular diseases in fetal origins. This study determined the influence of maternal intake of high sucrose (HS) during pregnancy on vessel tone, intracellular Ca(2+) ([Ca(2+)](i)), K(+) channels, especially large-conductance Ca(2+)-activated K(+) channels (BK), in mesenteric arteries in the offspring rats exposed to prenatal HS. Vessel tension and [Ca(2+)](i) induced by angiotensin II were higher in the small mesenteric arteries of the HS offspring. In the vascular smooth muscle cells (VSMCs) from the HS offspring, electrophysiological studies showed depressed BK current density and depolarized membrane. Western blot showed altered expressions of BK α-subunits, AT1 and AT2 receptors in mesenteric arteries. The results suggest that decreased BK channel activity and depolarized membrane potential in the VSMCs partly contributed to the increased vessel tone and [Ca(2+)](i) in the HS offspring, adding new information for understanding mechanisms in vascular malfunctions in fetal origins, and novel insights for early prevention and treatments against such vascular diseases.