Vesicles exit from

PMN binding to and migration across endothelium initiates a sequence of events that resembles that following histamine treatment [14,30], namely, an increase in the permeability of the EC monolayer. For anionic plasma macro-molecules, theplasmalemmal vesicles and bansendothdial channels are suitable candidates for exit from the vessel lumen. Indeed, receptor-mediated tranacytosis of insulin and transferrin has been identified for brain capillaries [31—33], The insulin curriers have nut yet been idoitified, but it is speculated that they could be coaled vesicles and/or plasmalemmal vesicles. Transferrin [341 as well as ceruloplasmin [33,36] binding has been localized to coated pits and vesicles in the endothelium of bone marrow and liver capillary endothelium, respectively. 

Large, non-lipid-soluble molecules may cross the capillary wall by transcytosis. This mechanism involves the transport of vesicles from one side of the capillary wall to the other. Many hormones, including the catecholamines and those derived from proteins, exit the capillaries and enter their target tissues by way of transcytosis. 

Figure 4.34 Schematic representation of one apparent mechanism for exocytotic release of secretory vesicle contents, (a) Vesicles assemble into a chain through ball-and-socket interaction. The exit vesicle interacts with apical plasma membrane via a vesicle depression, (b) Linked vesicles fuse together, apparently by disintegration of membrane in areas of fusion, resulting in the formation of a continuum with the alveolar lumen, (c) Emptying of the vesicular chain appears to result in collapse and subsequent fragmentation of the membrane. (From Keenan...

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