Portal hypertension and angiogenesis

The pathophysiological background of the haemodynamic changes in chronic po rtal hypertension is still only partly understood. An important factor is t he so-called "forward theory", explaining the systemic and especially splan chnic 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 hypertensio n show increased angiogenesis and NO appears to be a mediator of this findi ng. The interaction(s) of NO with other angiogenic molecules is now being e xplored. A better understanding of these structural vascular changes map he lp to develop new therapeutic strategies in the future.