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Sensors and Sensing in Biology and Engineering pp 197–212Cite as

Mechanism of Shear Stress-Induced Coronary Microvascular Dilation

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Abstract

In the coronary circulation, fluid shear stress acts as an important, moment-to-moment regulator of vascular resistance. Coronary microvessels display profound vasodilation to increased shear stress, a response shown to be mediated by endothelium-dependent release of nitric oxide. However, the sensory transduction mechanism and the intracellular signaling pathway by which shear stress stimulates release of nitric oxide in endothelial cells is not completely understood. In this chapter, the involvement of cytoskeleton, integrin/focal adhesion proteins, protein kinases, membrane potassium channels and calcium mobilization in endothelial activation and vasodilation to elevated shear stress is discussed. The vasomotor regulation by shear stress in the coronary microcirculation is specially emphasized.

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Authors
  1. Lih Kuo
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  2. Travis W. Hein
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Editors and Affiliations

  1. Biocenter, Institute of Zoology — Neurobiology, University of Vienna, Austria

    Friedrich G. Barth

  2. Department of Mechanical and Aerospace Engineering, University of Virginia, Charlottesville, VA, USA

    Joseph A. C. Humphrey

  3. Department of Physiology, University of Arizona, Tucson, AZ, USA

    Timothy W. Secomb

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Kuo, L., Hein, T.W. (2003). Mechanism of Shear Stress-Induced Coronary Microvascular Dilation. In: Barth, F.G., Humphrey, J.A.C., Secomb, T.W. (eds) Sensors and Sensing in Biology and Engineering. Springer, Vienna. https://doi.org/10.1007/978-3-7091-6025-1_14

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