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Regulation of Platelet Function by Flow-Induced Release of Endothelial Autacoids

  • Rudi Busse
  • Ingrid Fleming
Part of the Clinical Physiology Series book series (CLINPHY)

Abstract

Under normal conditions, the vascular endothelium significantly contributes to the control of cardiovascular homeostasis by maintaining platelets in an inactive resting state. In response to vessel wall damage, platelets undergo a shape change, adhesion, aggregation, and degranulation to release a number of biologically active substances, culminating in the formation of a thrombus (49). In addition, substances released from activated platelets affect the contractile function of vascular smooth muscle cells and can modulate their growth as well as that of endothelial cells. During the last 2 decades it has become apparent that endothelial cells respond to platelet-derived factors by producing a number of autacoids that modulate not only endothelial function, but also that of platelets and vascular smooth muscle cells. Of these autacoids, prostacyclin (PGI2) and nitric oxide (NO) appear to play an active role in the prevention of thrombus formation during flow through the normal circulatory system (67). Indeed the physical force of the shear stress exerted on endothelial cells by the flowing blood has been shown to be an effective stimulus for production and release of these autacoids (12). This same force, acting on platelets, can lead to their activation under certain hemodynamic conditions, such as arterial stenosis or excessively high flow rates (81, 103, 107, 116). Thus, it is obvious that changes in the functional state of either platelets or endothelial cells will have dramatic consequences on cardiovascular homeostasis. In this review we will focus on the effects of endothelium-derived PGI2 and NO on platelets, the synergism between these two autacoids, and the impact of decreased endothelial autacoid production on platelet function. A number of recent reviews contain more detailed information on signal transduction pathways in platelets and endothelial cells (41, 68, 92, 101).

Keywords

Nitric Oxide Endothelial Cell Platelet Activation Platelet Function Myosin Light Chain Kinase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© American Physiological Society 1995

Authors and Affiliations

  • Rudi Busse
  • Ingrid Fleming

There are no affiliations available

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