INCREASED BASAL ARTERIAL SMOOTH-MUSCLE GLUCOSE-TRANSPORT IN THE ZUCKER RAT

Insulin has recently been reported to stimulate glucose transport in v ascular smooth muscle cells (VSMC). This observation suggests a role f or this hormone in hypertension associated with insulin resistance. To determine whether VSMC glucose transport abnormalities exist in a sta te of insulin resistance, we studied basal and insulin-stimulated gluc ose transport in VSMC derived from Zucker lean (normotensive, insulin sensitive) and obese (hypertensive, insulin resistant) rats. Basal glu cose transport, as measured by tracer quantities of [H-3]2-deoxyglucos e, was 4.2 +/- 0.8 and 7.4 +/- 0.9 fmol/10(6) cells/min for lean and o bese cells, respectively (P < .05). Kinetic analyses utilizing variabl e concentrations of unlabeled 2-deoxyglucose in the media revealed tha t increased transport in the obese rat was due to an increased V-max o f the transporter system: V-max = 5.9 +/- 0.8 and 12.1 +/- 1.2 fmol/10 (6) cells/min for lean and obese cells, respectively (P < .05); no cha nges in K-m were noted for the two populations: K-m = 1.14 +/- 0.24 an d 0.96 +/- 0.10 mmol/L. Insulin (10 mu U/mL) increased the V-max of th e transporter in both preparations, but greater stimulation was seen i n the lean VSMC: 32 +/- 4.8% v 11.5 +/- 2.1% (P < .05). Insulin had no effect on the K-m of the transporter in either strain. These data sug gest that increased basal glucose transport in obese VSMC may predispo se the vessel to increased glucose-mediated events, while blunted insu lin-stimulated glucose transport in these cells mirrors insulin-resist ant glucose disposal in other tissues of the obese rat.