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RESEARCH COMMUNICATION |
a Department of Internal Medicine, University Hospital Benjamin Franklin, Free University Berlin, 12200 Berlin, Germany
Activation of ion channels and the increase in intracellular Ca2+ concentration [Ca2+]i play a key role in endothelial responses to hemodynamic forces and subsequent vasoregulation. In bovine aortic endothelial cells subjected to shear stress in a parallel flow chamber, we demonstrate shear stress activation of hyperpolarizing K+ currents that occur simultaneously with oscillating increases of [Ca2+]i. Oscillating K+ currents, also known as spontaneous transient outward currents (STOC), were regulated in frequency and amplitude by the rate of shear stress in a range from 5 to 18 dyn/cm2. Activation of STOC depended on Ca2+ influx; current depended on the extracellular Ca2+ concentration and was blocked by 50 µM Gd3+. Emptying of Ca2+ stores by BHQ abolished current responses to shear stress. STOC activation was significantly reduced by cell dialysis with ryanodine (20 µM), but not heparin (200 µg/ml). Shear stress-induced STOC activation was also observed in the intact endothelium. The endothelial response to shear stress involves oscillating [Ca2+]i increase and STOC activation, which depend on Ca2+ influx-induced Ca2+ release from ryanodine-sensitive stores, demonstrating a new signaling pathway in endothelial mechanotransduction.—Hoyer, J., Köhler, R., Distler, A. Mechanosensitive Ca2+ oscillations and STOC activation in endothelial cells. FASEB J. 12, 359–366 (1998)
Key Words: shear stress • spontaneous transient outward currents • intracellular calcium • ryanodine • bovine aortic endothelial cells
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