Uterine venous permeability in the rat is altered in response to pregnancy, vascular endothelial growth factor, and venous constriction.

Venoarterial communication is a potential short-loop signaling pathway for the local control of uteroplacental perfusion. As this pathway is permeability-dependent, this study investigated the effects of molecular weight, gestation, vascular endothelial growth factor (VEGF), wall tension, and constriction on solute flux across the venous wall. Experiments utilized fluorimetry to quantitate solute flux (3- and 70-kDa dextran) in isolated segments of uterine vein from virgin (NP) and late-pregnant (LP; day 20) rats as a function of endothelial surface area and time. Uterine veins were > 10-fold more permeable to the 3- versus 70-kDa dextran in both NP and LP groups. Flux was increased during gestation ( 2.5-fold), and by VEGF (NP, 3 kDa: 3.3-fold, 70 kDa: 4.8-fold; LP, 3-kDa: 3.3-fold, 70 kDa: 7.4-fold). Permeability to the 3 kDa dextran correlated directly with wall tension (r2 = .74 in both groups), whereas permeability to both dextrans correlated inversely with constriction (NP: r2 = .85 and .76; LP: r2 = .89 and .79, respectively). Uterine veins demonstrate permeability to 3- and 70-kDa tracers resulting from molecular weight dependence and an apparent difference in transport mechanisms. Permeability is enhanced by gestational remodeling and subject to modulation by placental factors, indicating the presence of a regulated pathway for the transfer of molecules across the venous wall.