Vascular remodelling is a wide term which includes any change in the molecular and morphological structure of blood vessels whether physiological or pathological. In a wider sense it will include the development of blood vessels from precursor cells or vasculogenesis, the sprouting and non-sprouting (intussusception) of new blood vessels from the pre-existing ones (angiogenesis or neovascularisation) and the change in the proportions of the different cell stirps composing the vessel wall leading to either vessel enlargement (positive remodelling) or reduction (negative remodelling). From this wide perspective vascular remodelling occurs physiologically, during embryonic and fetal life, in the normal process of wound healing and in female reproductive cycle (uterus and ovary); and pathologically, in retinopathy of prematurity and diabetic retinopathies, in tumour growth and pulmonary and systemic arterial hypertension. Combinations of remodelling mechanisms are common in many pathological processes: thickening of the arterial walls is accompanied by formation of new blood vessels aimed to nourish the grown arterial layers. Among the many factors triggering and controlling vascular remodelling, hypoxia and the transcriptional regulator of hypoxia-responsive genes, hypoxia inducible factor, are of prime importance in processes such as tumour vascularisation and pulmonary circulation remodelling. In my presentation I shall review some of the general factors involved in vascular remodelling in pulmonary circulation. Recent findings in models of sustained hypoxia, animal models of chronic obstructive pulmonary disease and perinatal hyperoxia shall be presented.

Supported by Grants BFU2004-06394 (DGICYT), FISS grant PI042462 (FIss) and VA011C05 (JCyL).