J Biol Chem, Vol. 274, Issue 36, 25250-25253, September 3, 1999

Effect of Glucose on Endothelin-1-induced Calcium Transients in Cultured Bovine Retinal Pericytes

Ann McGinty, C. Norman Scholfield^§, Wei-Hua Liu, Paul Anderson, D. E. Elaine Hoey, and Elisabeth R. Trimble^¶

From the  Department of Clinical Biochemistry and the ^§ School of Biomedical Science, Queen's University of Belfast and the ^¶ Department of Clinical Biochemistry, Royal Group of Hospitals, Belfast BT12 6BA, United Kingdom

Published work has shown that endothelin-1-induced contractility of bovine retinal pericytes is reduced after culture in high concentrations of glucose. The purpose of the present study was to establish the profile of endothelin-1-induced calcium transients in pericytes and to identify changes occurring after culture in high concentrations of glucose. Glucose had no effect on basal levels of cytosolic calcium or on endothelin-1-induced calcium release from intracellular stores. However, influx of calcium from the extracellular medium after endothelin-1 stimulation was reduced in pericytes that had been cultured in 25 mM D-glucose. L-type Ca²⁺ currents were identified by patch clamping. The L-type Ca²⁺ channel agonist, ()-Bay K8644, caused less influx of calcium from the extracellular medium in pericytes that had been cultured in 25 mM D-glucose than in those cultured with 5 mM D-glucose. However, 3-O-methylglucose, a nonmetabolizable analogue of glucose which can cause glycation, had similar effects to those of high concentrations of glucose. The results suggest that reduced function of the L-type Ca²⁺ channel that occurs in bovine retinal pericytes after culture in high concentrations of D-glucose is probably due to glycation of a channel protein.