Abstract
Vasomotion of large arteries can be brought about by two different mechanisms:
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1.)
Direct effects of various agonists or transmitters on the smooth muscle cells, effecting either contractions or relaxation depending on the induced level of myoplasmic free calcium (which in turn is largely controlled by the concentration of cGMP and the activity of guanylate cyclase).
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2.)
Vasomotion can also result from indirect effects on vascular smooth muscle. Various agonists and physico-chemical stimuli act on the endothelial surface to release, via the abluminal side, a vasomotor signal to the adjacent vasculature. With regard to endothelium-mediated vasomotion, there is convincing evidence for the presence and significance of an endothelium-derived relaxant factor (EDRF). However there is much less evidence for endothelium-mediated vasoconstriction. Endothelium-mediated relaxation was first shown by Furchgott and Zawadzki in 1980, using a sandwich technique in which EDRF could diffuse from a segment with stimulated endothelium to a non-endothelium-containing indicator vessel segment.
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Bassenge, E., Pohl, U. (1986). Two Principles of Large Artery Dilation: Indirect Endothelium-Mediated and Direct Smooth Muscle Relaxation. In: Magro, A., Osswald, W., Reis, D., Vanhoutte, P. (eds) Central and Peripheral Mechanisms of Cardiovascular Regulation. NATO ASI Series, vol 109. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9471-0_7
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