Abstract
The importance accorded to platelet function in the pathogenesis of hypertension and its complications rests on many considerations. Platelets may be argued to play a patho-physiological role, since they produce vasoconstrictors (e.g., thromboxane, TXA2, and serotonin, 5-HT) and growth factors (platelet-derived growth factor, PDGF), as well as participating actively in the development of thromboembolic complications. On the other hand, vasoconstrictor factors, such as epineprine, angiotensin II, and vasopressin, are capable to activate or sensitize the platelets by acting on specific receptors. In hypertension, increased shear stress on the vessel wall and the resulting endothelial damage can also activate the platelets, with important consequences in the onset and continuation of the atherosclerotic process. Finally, if the hypothesis is accepted that essential hypertension is characterized by a widespread genetically determined cellular abnormality, this could affect not only the smooth muscle cells of the blood vessels, but also other cells such as platelets.
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© 1991 Springer-Verlag Berlin • Heidelberg
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Lechi, A. et al. (1991). Platelet Abnormalities in Human Hypertension. In: Bruschi, G., Borghetti, A. (eds) Cellular Aspects of Hypertension. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-00983-3_23
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DOI: https://doi.org/10.1007/978-3-662-00983-3_23
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