Vascular endothelium responds to shear stress due to blood flow by releasing nitric oxide (NO). Deficiencies in this vasodilator has been implicated in diseases such as essential hypertension, coronary artery insufficiency and chronic heart failure. However, Because of the short T1/2 of this free radical (<6 Sec.) the mechanism by which shear stress induces NO release and the components of the shear stress activated pathway are unknown. We propose to investigate this mechanism using our unique published porphyrin/Nafion coated carbon fiber microsensor for on line detection of NO combined with fura-2 fluorescence and patchclamp techniques for monitoring Ca2+ flux. Shear stress elevates cytosolic Ca2+ ([Ca2+]i) which is necessary for the activation of Ca2+
| Kanai, A J; Mesaros, S; Finkel, M S et al. (1997) Beta-adrenergic regulation of constitutive nitric oxide synthase in cardiac myocytes. Am J Physiol 273:C1371-7 |
| Kanai, A J; Strauss, H C; Truskey, G A et al. (1995) Shear stress induces ATP-independent transient nitric oxide release from vascular endothelial cells, measured directly with a porphyrinic microsensor. Circ Res 77:284-93 |
