Sodium-coupled glucose transporter as a functional glucose sensor of retinal microvascular circulation

To clarify the function of the Na+-coupled glucose transporter in the regul ation of cellular tone of cultured retinal pericytes, we investigated the e ffects of extracellular glucose concentration on cell size. The surface are a and diameter of cultured bovine retinal pericytes under different glucose concentrations were measured by using a light microscope with a digital ca mera. We also examined the effects of extracellular Na+ and Ca2+, inhibitor s of the Na+-coupled glucose transporter and Na+-Ca2+ exchanger, a Ca2+ cha nnel blocker, and nonmetabolizable sugars on cell size, The surface area an d diameter of the cells changed according to extracellular glucose concentr ations. alpha -Methyl glucoside, which enters the cell through the Na+-coup led glucose transporter, induced cellular contraction. However, the cells d id not contract in response to 2-deoxyglucose, which enters the cell throug h a facilitated glucose transporter. Glucose-induced cellular contraction w as abolished in the absence of extracellular Na+ and Ca2+. Moreover, phlori zin, an inhibitor of the Na+-coupled glucose transporter, and 2 ' ,4 ' -dic hlorobenzamil-HCl, an inhibitor of the Na+-Ca2+ exchanger, also abolished g lucose-induced cellular contraction, whereas nicardipine, a Ca2+ channel bl ocker, did not. Our results indicate that high extracellular glucose concen trations induce contraction of bovine retinal pericytes via Na+ entry throu gh a Na+-coupled glucose transporter, suggesting that the Na+-coupled gluco se transporter may act as a functional glucose sensor of retinal microvascu lar circulation.