title: [Portal hypertension and angiogenesis].
abstract: The pathophysiological background of the haemodynamic changes in chronic portal hypertension is still only partly understood. An important factor is the so-called "forward theory", explaining the systemic and especially splanchnic vasodilation observed. Nitric oxide (NO) is an important mediator of this vasodilatory state. Structural as well as vascular changes seem to be causative factors in this vasodilation. These alterations can be studied by a newly-developed in vivo angiogenesis assay. Rats with portal hypertension show increased angiogenesis and NO appears to be a mediator of this finding. The interaction(s) of NO with other angiogenic molecules is now being explored. A better understanding of these structural vascular changes may help to develop new therapeutic strategies in the future.
authors.affiliation: Abteilung für Gastroenterologie, Kantonsspital Basel.
authors.forename: M
authors.initials: M
authors.lastname: Stumm
authors.forename: C
authors.initials: C
authors.lastname: Sieber
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D006133:Growth Substances / Q000502:physiology; D006801:Humans; D006975:Hypertension, Portal / Q000503:physiopathology*; D009389:Neovascularization, Pathologic / Q000503:physiopathology*; D009569:Nitric Oxide / Q000502:physiology; D051381:Rats; D013152:Splanchnic Circulation / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
chemical_list: D006133:Growth Substances; D009569:Nitric Oxide