Journal List > Korean J Gastroenterol > v.56(3) > 1006704

Kim and Baik: Pathophysiology of Portal Hypertension, What's New?

Abstract

Portal hypertension (PHT) is associated with changes in the intrahepatic, systemic and portosystemic collateral circulations. Alteration in vasoreactivity (vasodilation and vasoconstriction) plays a central role in the pathogenesis of PHT by contributing to increased intrahepatic resistance, hyperdynamic circulation and the expansion of the collateral circulation. PHT is also importantly characterized by changes in vascular structure; termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the sprouting of new blood vessels, also occurs in PHT, especially in the expansion of the portosystemic collateral circulation. These complementary processes of vasoreactivity, vascular remodeling and angiogenesis represent important targets in the research for the treatment of portal hypertension.

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Fig. 1.
Hepatic stellate cell (HSC) activation. In quiescent state, HSC do not contract (A), however in activated state, the number and contractility of HSC increase which induce the change of sinusoidal structure and intrahepatic resistance.
kjg-56-129f1.tif
Fig. 2.
Pathogenesis of hyperdynamic circulation. VEGF, vascular endothelial growth factor; eNOS, endothelial nitric oxide synthase; RAA system, renin- angiotensin-aldosterone system; ADH, antidiuretic hormone; TNF-α, tumor necrosis factoralpha.
kjg-56-129f2.tif
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