It should be clear from the previous sections that a large number of substances can induce the contraction or relaxation of vascular smooth muscle. Many of these substances do so by acting directly on the arteriolar smooth muscle, but others act indirectly via the en-dothelial cells adjacent to the smooth muscle. En-dothelial cells, in response to these latter substances as well as certain mechanical stimuli, secrete several paracrine agents that diffuse to the adjacent vascular smooth muscle and induce either relaxation or contraction, resulting in vasodilation or vasoconstriction, respectively.
Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth Edition
Circulation CHAPTER FOURTEEN
One very important paracrine vasodilator released by endothelial cells is nitric oxide; note that we are dealing here with nitric oxide released from endothelial cells, not nerve endings as described in an earlier section. [Before the identity of the vasodilator paracrine agent released by the endothelium was determined to be nitric oxide, it was called endothelium-derived relaxing factor (EDRF), and this name is still often used because there may be substances other than nitric oxide that also fit this general definition.] Nitric oxide is released continuously in significant amounts by endothelial cells in the arterioles and contributes to arteriolar vasodilation in the basal state. In addition, its secretion is rapidly and markedly increased in response to a large number of the chemical mediators involved in both reflex and local control of arterioles. For example, nitric oxide release is stimulated by bradykinin and histamine, substances produced locally during inflammation (Chapter 20).
Another vasodilator released by endothelial cells is the eicosanoid prostacyclin (PGI2). Unlike the case for nitric oxide, there is little basal secretion of PGI2, but secretion can increase markedly in response to various inputs. The roles of PGI2 in the vascular responses to blood clotting are described in Section G of this chapter.
One of the important vasoconstrictor paracrine agents released by endothelial cells in response to certain mechanical and chemical stimuli is endothelin-1 (ET-1). ET-1 is a member of the endothelin family of peptide paracrine agents secreted by a variety of cells in diverse tissues, including the brain, kidneys, and lungs. Not only does ET-1 serve as a paracrine agent but under certain circumstances it can also achieve high enough concentrations in the blood to serve as a hormone, causing widespread arteriolar vasoconstriction.
This discussion has so far focused only on arteri-oles. However, endothelial cells in arteries can also secrete various paracrine agents that influence the arteries' smooth muscle and, hence, their diameters and resistances to flow. The force exerted on the inner surface of the arterial wall, specifically on the endothelial cells, by the flowing blood is termed shear stress; it increases as the blood flow through the vessel increases. In response to this increased shear stress, arterial en-dothelium releases PGI2, increased amounts of nitric oxide, and less ET-1. All these changes cause the arterial vascular smooth muscle to relax and the artery to dilate. This flow-induced arterial vasodilation (which should be distinguished from arteriolar flow autoregulation) may be important in remodeling of arteries and in optimizing the blood supply to tissues under certain conditions.
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