Date of Award


Degree Name

Biomedical Sciences


Joan C. Edwards School of Medicine

Type of Degree


Document Type


First Advisor

Elsa Mangiarua

Second Advisor

Donald Primerano

Third Advisor

Vernon Reichenbecher

Fourth Advisor

Gary Wright

Fifth Advisor

William McCumbee

Sixth Advisor

Leonard J. Deutsch


Glucose transport was assessed in vascular smooth muscle (VSM) cells by measuring the uptake of a radiolabeled non-metabolizable glucose analog, [3H]-2-deoxglucose. VSM cells, isolated from rat aortae by enzymatic digestion, were maintained in culture in Dulbecco's Modified Eagle Medium supplemented with 10% newborn calf serum at 37°C with 5% CO2 and air. Angiotensin II (AU) increased glucose transport by 84%. Significant stimulation occurred by two hours of exposure with the maximum effect being observed between six and eight hours. All effects were concentration dependent with a threshold response being detected at 0.1 nM. All-stimulated transport was blocked by an AU receptor antagonist. AII stimulation was shown to require protein synthesis. A specific protein synthesized in response to AII stimulation was the GLUT 1 glucose transporter as assessed by western blot analysis, using an antibody generated against the carboxyl terminus of the GLUT 1 transporter. Protein kinase C (PKC) stimulation with phorbol esters significantly increased glucose uptake. The majority of evidence from PKC inhibition and downregulation studies however, suggest AU is capable of stimulating glucose transport through a PKC-independent mechanism. Extracellular calcium and calmodulin appear to be required for AU stimulation of glucose transport. Hyperglycemic conditions reduced basal glucose transport. The maximum rate of All-stimulated transport was not appreciably altered by the glycemic state; however, the relative effectiveness of AII at different concentrations of glucose varied with media glucose concentration.