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For example, while the laminin A chain is involved in the initial attachment of endothelial cells, the B, chain mediates cellular reorganization and reorientation within hollow tubes. In addition, the basement membrane stores bFGF in duced, for instance, by stretching.This mechanism could explain growth of vessels in skeletal muscles exposed to stretch. It might also contribute to capillary growth in hearts with more vigorous contractions during systole, whether in hyperthyroidism, during longterm brady cardial pacing, or with dobutamine treatment. It seems likely therefore that even though mechan ical factors connected with increased blood flow are crucial in the stimulation of capillary growth under most physiological and some pathological circumstances, capillary growth in the heart is more probably due to activation of growth fac tors.However, mechani cal factors such as S tretch of the capil lary wall possibly play an importan trole even in the heart.Be cause vascular growth occurs in normal adult tissues rather rarely, factors limiting it must be present at all times.The most obvious limiting factor is inhibition of capillary growth by pericytes and of growth in larger vessels by mutual interaction between endothelial and vascular smooth Cabazitaxel muscle cells.A highmolecularweight factor inhibiting growth of vascular smooth muscle cells was isolated from the medium used for cultivation of bovine aortic endothelial cells. Proliferation of smooth muscle cells in rab bit ear artery was limited by pretreatment with dipyri damole. Heparin has a simi lar role: it is possibly involved in the stimulation of capil lary growth but inhibits growth of smooth muscle cells both in vitro. It is known that cartilage differentiation inhibits angiogenesis during development. There are numerous reports on the inhibitory effect on growth of vessels or endothelial cells of cartilage or its extracts, as well as extracts from other avascular tis sues like the vitreous. However, it is very unlikely that any of these factors would play a role in the inhibition of growth in skeletal or cardiac muscles in the situations described.Similarly, it is not very likely that a combined effect of heparin and cortico steroids, a very potent inhibitor of vessel growth in tu mors or CAM, would limit angiogenesis in these two tissues.Real inhibition of vessel growth in cardiac or skele tal muscles was described only during development. There are several reports of capillary involution after a period of growth, during detraining. These could be Bexarotene explained by the return of blood flow to normal and thus the elimination of mechanical factors connected with it.However, longterm limita tion of bloodflow in skeletal muscles did not lead to loss of capillaries, although there was an indica tion of a diminished size of the whole muscle vascular bed. Unlike the heart, where there is obviously a loss of capillaries as well as an involution of larger ves sels in infarcted tissue, the development of collateral circulation in skeletal muscles may allow some, albeit limited, perfusion that could represent an adequate stimulus for the maintenance of capillary integrity.This is one of the reasons for the variability of the data on capillary supply in peripheral vascular diseases, which show no change.

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