Normalor Baseline Vascular Permeability

Hydraulic Conductivity—Lp

Lp of microvascular beds is heterogeneous under normal conditions, and the mechanisms that regulate baseline permeability are not clear. The number of tight junction strands is greater in vascular beds with lower Lp and Ps (e.g., blood-brain barrier). Some signaling pathways have been shown to be able to increase junctional strand number in endothelial cells in culture and to decrease Lp in vivo. Intracellular cAMP can stimulate the formation of tight junction strands by PKA-mediated phosphorylation of junctional associated proteins. The degree of filling of Ca2+ stores in the endothelial cells may regulate baseline Lp, although the link between Ca2+ stores and cAMP mediated pathways has not yet been determined. Nitric oxide has been implicated, since inhibition of NO synthase results in a transient increase of baseline Lp. The presence of fenestrations will result in a much greater baseline Lp, as is seen in renal, salivary, and synovial capillary beds, to name a few.

Solute Permeability—Ps

Little is known of the intracellular signaling cascades that regulate normal Ps, but for small solutes this is likely to be the same as that governing L For larger molecular weight solutes, despite many decades of research, it is still not clear what are the contributions to basal Ps of the different signal transduction pathways.

Oncotic Reflection Coefficient—o

Regulation of reflection coefficient is dependent on the functional pore radius. Diaphragms in fenestrae decrease the pore radius such that fenestrated endothelium has a high o despite a high Lp. Little is known concerning the signaling pathways that regulate fenestrations, although the isolation of the protein that forms diaphragms across fenestrae of caveolae—PV-1—should mean that regulation of fenestrations will become more clearly understood.

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