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In fact, the degree of pruning increases as the pressure drop increases (Skalak and Price, 1996). Pruning and remodeling of the vascular network may be stimulated by tissue-derived signaling molecules and blood flow conditions (e.g. wall-shear stress and pressure). Although the morphological hallmarks of IMG and IAR, crucial mechanisms for generating and expanding a capillary network, were frequently observed in capillaries and terminal microvessels with diameters selleck microvessels (Djonov et al., 2002). This process hence was termed intussusceptive branching remodeling (IBR). An interesting model of vascular pruning is provided by modification of pulmonary vascularization under certain conditions (Howell et al., 2003). Chronic hypoxia caused by migration of native sea-level dwellers to high altitude or chronic lung disease leads to the development of increased pulmonary vascular resistance and pulmonary hypertension (Meyrick and Reid, 1978?and?Hopkins and McLoughlin, 2002). The structural changes that are thought to underlie the increased vascular resistance can be broadly classified into two processes: firstly, remodeling of the walls of the see more pulmonary resistance vessels and, secondly, pruning in the total number of blood vessels in the lung (Meyrick and Reid, 1978?and?Rabinovitch et al., 1979). The structural changes include muscularisation of non-muscular arterioles, increased medial thickness of muscular arterioles, adventitial hypertrophy and deposition of additional matrix components, including collagen and elastin, in the vascular walls (Rabinovitch et al., 1979; Stenmark and Mecham, 1977). The second major structural alteration caused by chronic hypoxia is loss of small blood vessels, which is said to increase vascular resistance by reducing the extent of parallel vascular pathways (Hislop and Reid, 1976, Hislop and Reid, 1977?and?Rabinovitch et al., SAR1B 1979). In another vascular system, the retina, oxygen supply is regarded as a key factor in blood vessel pruning. Earlier studies have highlighted the key role of oxygen and VEGF in the formation and remodeling of the retina vasculature (Stone and Maslim, 1997?and?Dorrell and Friedlander, 2006). In addition to preventing new vessel growth, hyperoxia suppresses VEGF production and leads to obliteration by apoptosis of already formed vessels (Stone et al., 1995). This suggests that vascular pruning accompanying natural remodeling is caused by hyperoxia upon the onset of flow through the newly formed vascular system. Exposure to hyperoxia leads to excessive regression of capillaries, while arteries become refractory to this insult (Benjamin et al., 1998).