Decreased Ca2+ influx into the endothelium contributes to the decrease in endothelium-dependent relaxation in the aorta of streptozotocin-induced diabetic mice.

Experiments were designed to investigate the role of Ca2+ influx into the endothelium in the relaxation of mouse aorta caused by acetylcholine (ACh) in streptozotocin (STZ)-induced diabetic and age-matched control mice. When Ca2+ was added to the bath, Ca2+ caused a transient contraction followed by relaxation in Ca(2+)-free medium containing 2 x 10(-6) M prostaglandin F2 alpha (PGF2 alpha) and 10(-5) M ACh in the control experiments. On the other hand, Ca2+ showed a long lasting contraction in STZ-induced diabetic rats. These results suggest that influx of Ca2+ into the endothelium is significantly attenuated in the diabetic vessels, and production or release of relaxing factor is markedly decreased.