Plasmalemmal vacuolar type H+-ATPase (pmV-ATPase) is decreased in microvascular coronary endothelial cells (MCEC) from an insulin dependent diabetic model (BBd).

Complications of diabetes involve abnormalities in blood flow regulation, microvascular proliferation and angiogenesis. Because intracellular pH (pHin) regulates cell growth, secretion, and cell motility/ migration, we examined if MCEC from the spontaneously diabetic BB rat (BBd) have altered pHin regulation. Cells from BBd and non-diabetic (BBn) rats were grown on glass cover slips and were intracellularly loaded with the pH fluorescent indicator SNARF-I. The steady-state pHin was significantly lower in the BBd than in BBn by ca. 0.1 pH unit regardless of the HCO3- concentration, suggesting that the differences were not due to HCO3--transport mechanisms. Acid loading experiments revealed similar levels of acidification in both cell types with BBn cells recovering faster than BBd, regardless of the presence or absence of Na+ and HCO3-. There were no differences in buffering capacity between BBn and BBd cells. In the absence of Na+, proton fluxes (JH+; mM/min) were two-fold higher in BBn man in BBd and were suppressed by V-H+-ATPase inhibitors. The data suggest that a dysfunction of pmV-ATPase is important in diabetes.

Plasmalemmal vacuolar type H+-ATPase (pmV-ATPase) is decreased in microvascular coronary endothelial cells (MCEC) from an insulin dependent diabetic model (BBd). Academic Article