Invited Symposium: Hypertension III: Flow-Induced Vascular Remodeling
It has been known for more than a century that the size of the lumen of a vessel depends on the rate of blood flow, but before the advent of molecular and cellular techniques, little was known about the mechanism of this relationship. With the discovery of the role of the endothelium in this process, experiments have been performed to explore the signaling pathway from initial mechanotransduction of shear stress to the final remodeling of the media around the larger lumen. In response to increases in shear stress, endothelial cells release nitric oxide and prostacyclin to promote vasodilatation and inhibit platelet aggregation. The resultant increase in circumferential wall stress may play a key role in transmission of the growth signal from the endothelium to the medial smooth muscle cells. In hypertension the arterioles undergo inward, eutrophic remodeling whereby they have the same medial mass rearranged around a smaller lumen. At the initiation of hypertension, the arterioles are severely constricted. Wall shear stress increases in the constricted arterioles, but endothelial dysfunction reduces the release of nitric oxide and uncouples the shear stress signaling pathway for lumenal expansion. As a result, the chronically smaller lumen becomes a structural adaptation to the elevated blood pressure and arteriolar tone returns toward control levels.
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|Prewitt, R.; (1998). Blood Flow-Induced Vascular Remodeling and Hypertension. Presented at INABIS '98 - 5th Internet World Congress on Biomedical Sciences at McMaster University, Canada, Dec 7-16th. Invited Symposium. Available at URL http://www.mcmaster.ca/inabis98/prewitt/prewitt0768/index.html|
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